Immunology
Quiz yourself by thinking what should be in
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| Four types of defensive barriers in Innate immunity: | show 🗑
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| show | 1) Present intrinsically without previous stimulation
2) Limited specificity for shared structures of microbes
3) Are not enhanced in activity by repeated exposure
4) Limited diversity of expression
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| show | 1) Lymphocytes
2) APCs (Macrophages, B cells, and dendritic cells)
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| show | 1) Specifity
2) Diversity
3) Enhanced with repeated exposure (memory)
4) Self/non self recognition
5) Self limiting
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| show | Phagocytosis
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| Antibodies activate: | show 🗑
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| show | Both
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| show | Opsonization
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| show | 1) Lymphoid - B, T cells/NK cells
2) Myeloid
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| show | Kidney bean shaped nucleus
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| show | Ruffled membrane
Cytoplasm with vacuoles and vesicles
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| show | Phagocytic
Differentiate into tissue macrophages
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| show | Phagocytic
Cytokine Secretion
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| show | Long cytoplasmic arms
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| show | Antigen capture, transport, and presentation
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| How are neutrophils identified? | show 🗑
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| What is the function of neutrophils? | show 🗑
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| How are eosinophils identified? | show 🗑
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| What is the function of eosinophils? | show 🗑
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| show | Bilobed nucleus
Large blue granules
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| show | Non phagocytic
Release pharmacologic substances during allergic responses
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| show | Small nucleus
Large blue granules in cytoplasm
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| show | Release of granules containing histamine
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| Identification of lymphocytes: | show 🗑
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| Function of lymphocytes: | show 🗑
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| show | Kill tumor/virus cell targets
Kill antibody coated cells
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| show | Small dark/intensely staining nucleus
Golgi apparatus
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| show | Produce antibody
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| The naive B-cell antigen receptors are: | show 🗑
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| show | a and B chains
TCR
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| show | Two identical heavy chains
Two identical light chains
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| show | A hinge region
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| The hinge regions purpose is | show 🗑
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| show | The idiotype
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| How many idiotypes can be expressed per cell? | show 🗑
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| The molecule of the TCR is: | show 🗑
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| T cells recognize what type of antigens? | show 🗑
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| B cells recognize what type of antigens? | show 🗑
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| show | Ig-a, Ig-B
CD19
CD21
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| show | CD3
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| show | 2
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| show | 1
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| show | V and J
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| show | Inserts bases randomly at the junctions of V,D, and J
Increases variability
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| show | Tdt being active during the rearrangement of all gene segments in the formation of TCR
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| Once a functional product has been made: | show 🗑
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| show | Early stage T and B-cell development in ALL
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| show | Apoptosis
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| In the light chain, once a functional product has been achieved by one arrangement | show 🗑
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| show | Ensures that B and T cells synthesize only one specific antigen-receptor per cell
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| show | The RNA level
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| Somatic hypermutation occur in which type of cells? | show 🗑
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| show | Antigen-combining portion of the molecule
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| The amino acid sequences of all the remaining domains tend to make up the: | show 🗑
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| show | Kappa and delta
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| Which cells mediate allergic response? | show 🗑
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| Plasma cells are the end cells of: | show 🗑
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| What are the two chains of the TCR made up of? | show 🗑
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| What is the difference between light and heavy chain? | show 🗑
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| A germline B-lymphocyte possesses 200 distinct V region genes, 5 J region genes, and 2 isotypic possibilities to rearrange for its selection of light chain synthesis. How many idiotypes could be produced by combining this sequence with 1 heavy chain? | show 🗑
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| show | A) Allelic exclusion
B) Allelic codominance
C) Affinity maturation
D) Alternative RNA splicing
E) Somatic hypermutation
Answer: D
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| show | of the abnormal cells determines them to be extremely primitive B cells, which are CD 19+, HLA-DR+, and Tdt+. Which of the following best describes the status of IgG synthesis most likely in the cells?
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| show | Answer: E- Acute lymphoblastic Leukemia
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| A woman with AML is treated with chemotherapy and undergoes remission. The prognosis for relapse is high, bone marrow transplant is undergone in the first remission. | show 🗑
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| 2 year old boy with severe combined immunodeficiency disease. Normal cellularity of bone marrow Normal number of T cell precursors entering the thymus, but no normal T cells in peripheral blood Cells populating the thymus lack CD3 | show 🗑
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| show | 1) Bone marrow
2) Thymus
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| show | 1) Spleen
2) Lymphoid
3) MALT
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| show | Self-tolerance
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| show | Deletion of cells whose idiotype has too great an affinity for normal cellular molecules
Occurs in the bone marrow
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| show | Inactivation of cells whose idiotype has too great an affinity for normal cellular molecules
Occurs in the periphery
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| show | 1) Cortex -outer, full of immature T cells
2) Medulla - T cells passes it as they mature
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| show | Epithelial cells
Dendritic cells
Macrophages
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| show | TCR is designed to bind antigenic peptides and it must be confirmed that the TCR will recognize normal self antigens
Prevent autoimmunity
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| How is the selection process for developing thymocytes done? | show 🗑
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| MHC 1 gene poducts: | show 🗑
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| show | HLA-DP
HLA-DQ
HLA-DR
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| Class 1 cells are expressed in what fashion? | show 🗑
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| What makes up MHC 1 molecules? | show 🗑
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| show | all the nucleated cells of the body
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| show | Transport of the class 1 antigen to the cell surface
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| show | Codominant
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| show | APCs
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| MHC 2 molecules are made up of: | show 🗑
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| A groove that will accommodate peptides to be presented to the TCR is formed where? | show 🗑
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| show | Positive selection
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| Cells with useless receptors which refuse to bind self-MHC recieve: | show 🗑
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| show | Negative selection
Undergo apoptosis
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| show | CD4 and CD8
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| show | Stabilize the interaction between MHC and TCR
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| Cells express only CD8 if their TCR binds: | show 🗑
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| show | MHC2
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| CD4+ cells that recognize class 2 MHC | show 🗑
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| show | Cytoxic T cells
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| show | They die
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| 8-year old boy diagnosed with ALL. Flow cytometry is used to determine the immunophenotype of the malignant cells. Patients cells are evaluated with monoclonal Abs for MHC 2, CD19, and D34. High levels of flourescence with ALL of these markers | show 🗑
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| Blood from 8 year old boy analyzed by flow cytometry. these cells are treated with fluorescent-labeled Ab's to various cell surface markers before they were evaluated by flow cytometry. | show 🗑
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| Markers for identification of B lymphocytes: | show 🗑
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| 18 year old member of soccer team seen by a physician because of chest tightness and dyspnea on exertion. 15cm mediastinal mass is detected readiographically. 80% of WBCs in peripheral blood are small, abnormal with lobulated nuclei and scant cytoplasm. | show 🗑
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| show | What surface cell markers do you expect to find on the malignant cells?
A) CD4-,CD8-,TCR-
B) CD4-,CD8-,TCR+
C) CD4-,CD8+,TCR+
D) CD4+,CD8-,TCR+
E) CD4+,CD8+,TCR+
Answer: A
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| Herpes simplex viruses are extremely successful pathogens because they have a variety of immunologic evasion mechanisms. For example, both HSV1 and 2 depress the expression of MHC class 1 molecules on the surface of infected cells; | show 🗑
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| show | T cell areas
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| What structures make up the red pulp? | show 🗑
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| show | High endothelial venules
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| This migration of naive lymphocytes to the lymph nodes involves a multistep sequence of: | show 🗑
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| The initial low-affinity interaction between lymphocytes and adhesion molecules is mediated by: | show 🗑
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| L-selectins bind to: | show 🗑
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| Lymph node biopsy of 6 year old boy shows markedly decreased numbers of lymphocytes in the paracortical areas. | show 🗑
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| 65 year old woman involved in an automobile accident that necessitated the removal of her spleen | show 🗑
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| show | and paracortical areas. Absence of which of the following of leukocyte surface molecules could result in this clinical picture?
A) Adressins
B Chemokines
C) Ig family cell adhesion molecules
D) Integrins
E) L-selectins
Answer: E
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| show | Pathologists reports back that the mass is a lymph node with increases cells of the cortical area. Flourescent antisera to which of the cell surface markers is most likely to bind to these cells?
A) CD2
B) CD3
C) CD4
D) CD16
E) CD19
Answer: E
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| A radioactive tracer dye is injected SC into the forearm of an experimental subject. What is the first area of the first draining lymph node that would develop significant radioactivity? | show 🗑
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| show | 1) Foreign
2) Chemical complexity
3) MW of 5000-10000 K
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| show | an immune response
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| The portion of the immunogen that has 3D complementarity with the idiotype is: | show 🗑
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| show | More than one identical epitope
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| Molecules that possess only one epitope are called: | show 🗑
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| show | 1) Peptides
2) 10-20 aas
3) ONLY when presented to them in MHC
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| Drugs allergies can be induced with small doses of the drug because: | show 🗑
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| show | Acute inflammatory response
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| What is the first step of acute inflammatory response? | show 🗑
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| Cytokines increase expression of: | show 🗑
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| The first cell to bind to the inflamed endothelium: | show 🗑
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| show | Monocytes
Macrophages
Eosinophils
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| show | 1) Rolling
2) Activation of chemoattractants
3) Arrest and adhesion
4) Transendothelial migration
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| Details of the first Rolling step: | show 🗑
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| Details of the step involving activation by chemoattractants: | show 🗑
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| Details of arrest and adhesion: | show 🗑
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| show | The phagocyte extends pseudopodia through the vessel wall and extravasates into the tissue
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| show | *Rare autosomal recessive disease
*Absence of CD18 --> common B2 chain of a number of integrin molecules
*Inability of the leukocytes to undergo adhesion dependent migration into sites of inflammation
*Abcess and pus fomation do not occur
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| show | 1) IL-8
2) C5a
3) Fibrenopeptides
4) Leukotriene B4
5) Formyl methionyl peptides
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| Origin of chemokines: | show 🗑
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| Origin of C5a: | show 🗑
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| show | Endothelial damage --> acitvation of Hageman factor --> thrombin --> fibrin clot degradation
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| show | Membrane phospholipids of marophages, monocytes, neutrophils, mast cells --> arachadonic acid cascade --> lipoxygenase pathway
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| show | Released from microorganisms
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| Phagocytosis involves: | show 🗑
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| show | 1) IgG
2) C3b
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| The respiratory burst activates a: | show 🗑
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| show | 1) NADPH oxidase
2) Myeloperoxidase
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| Function of NADPH oxidase: | show 🗑
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| Function of Myeloperoxidase: | show 🗑
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| show | 1) Lysozyme --> digests bacterial cell walls by cleaving peptidoglycan
2) Defensins
3) Lactoferrin - chelates iron
4) Hydrolytic enzymes
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| Chronic granulomatous disease: | show 🗑
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| Rabbit hunter in Arkansas diagnosed with ulceroglandular tularemia and treated with streptomycin. Within a week, he returns to the hospital. The tularemic papule, lymphadenopathy, and bacteremia have resolved-> developed a raised, itching skin rash, fever | show 🗑
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| During WW2, when quinine was used as a prophylactic against malaria in soldiers, a small portion of soldiers developed blackwater fever (KD from the autoimmune effects of complement hemolysis). | show 🗑
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| show | The nitroblue tetrazolium dye reduction test is normal. What is the most likely defect in this child?
A) Absence of CCR4
B) Absence of CD18
C) Absence of IL-1
D) Absence of IL-4
E) Absence of TNF-a
Answer: B - LAD
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| Absence of CCR4 would cause: | show 🗑
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| show | Leukocyte Adhesion Deficiency
Inability of WBCs to migrate to sites of inflammation
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| Absence of IL-1 would cause: | show 🗑
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| show | Defects in the ability to mount a normal IgE Ab response
Development of TH2 from naive TH cells
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| show | Difficulty in acute and chronic response
Same as IL-1
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| 2 year old boy is admitted to the hospital for workup of a possible immunological disorder. History is remarkable for the occurrence of multiple skin infections. On examination, the child has cervical lymphadenopathy and mild hepatosplenomegaly. | show 🗑
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| show | 1) Staph
2) Pseudomonas
3) Candida
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| in animal experiments there are advantages to eliciting non-specific inflammation at the site of inoculation of antigen toward the ultimate development of protective immune response to that immunogen. Which of the following substances if introduced with | show 🗑
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| What is the function of APCs? | show 🗑
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| show | a and B chains
Invariant chain
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| show | Blocks the peptide binding groove so no normal peptides are accidentally attracted there
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| show | Endogenous pathway
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| show | N-terminal
These pepcytes are from the endogenous oathway
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| Proteins synthesized in the cell cytosol are routinely degraded in proteosomes and these are transported to into the ER by: | show 🗑
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| Does MHC 1 have an invariant chain? | show 🗑
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| Does MHC1 have B2 microglobulin? | show 🗑
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| show | Secondary lymphoid organs
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| Dendritics cells are: | show 🗑
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| What is the first signal for the naive T cell to begin its activation? | show 🗑
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| show | Co-stimulatory molecules on the APC secrete cytokine and induce the clonal expansion of T cells into effector and memory cells
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| show | CD4 --> which binds MHC2
CD8 --> MHC1
LFA-1 (Integrins) --> IgCAM-1
IgCAM (CD2) --> LFA-3
CD28 --> B7
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| What is the most important growth factor for T cells? | show 🗑
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| show | IL-2
IL-1
IL-6
TNF-a
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| show | Viral or bacterial proteins that cross-link the variable B domain of a TCR to an a-chain of a MHC 2 molecule
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| What function does the cross-linkage made by superantigens serve? | show 🗑
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| Which substances are over-produced by superantigen activation of T cells? | show 🗑
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| Which molecules tend to act as superantigens? | show 🗑
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| What are the effector mechanisms controlled by the TH cells? | show 🗑
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| show | MHC class 2 molecule deficiency
*Inherited autosomal recessive
*Increased susceptibility to infections
* CD4 deficiency
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| show | TH1
TH2
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| Microbes that stimulate a strong innate immune response with resultant production of IL-12 by macropages or IFN by Nk cells stimulate which TH cell? | show 🗑
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| Absense of such an innate immune stimuli stimulates production of: | show 🗑
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| In response to allergens which TH cell is stimulated? | show 🗑
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| show | IFN-y
TNF-B
IL-2
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| Which cytokines do TH2 cells produce? | show 🗑
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| Which cytokines inhibit TH2? | show 🗑
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| Which cytokines inhibit TH1? | show 🗑
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| Difference between tuberculoid and leptromatous leprosy: | show 🗑
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| show | but produce tissue damage. These patients have granulomas with elevated IL-2, IFN-y, and TNF-B. Which immune cells is responsible for this?
A) Cytotoxic T
B) Epitheloid
C) Macrophage
D) TH-1
E) TH2
Answer: D
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| Immunologic pathway that distinguishes the selection between the two forms of leprosy depends on the initial means of antigen presentation and different immune response. If these events elicit production of IL-4. IL-5, IL-6, and IL-10,lepromatous leprosy | show 🗑
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| 10 year old infant girl with signs of Pneumocystis carinii pneumonia. Peripheral blood tests demonstare age normal counts of CD 19+, but CD and CD4 depressed. Immunoelectrophoresis shows moderate hypogammaglobulinemia. Lymphocytes proliferate normally | show 🗑
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| show | How does the toxin responsible cause these signs?
A) Activates IL-1 homologue
B) Activates B cell polyclonally
C) Activates complement
D) Cross links MHC class 2 to TCRs
E) Stimulates neutrophils
Answer: D
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| show | Which of the following molecules would be the best choice for transfection of these tumor cells?
A) B7
B) CD2
C) CD4
D) CD28
E) LFA-1
Answer: A
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| show | Antibodies
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| show | Follicular areas of secondary lymphoid organs
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| show | Thymus-dependent antigens
Response to these molecules requires the direct contact of B cells with TH cells and their cytokines
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| What are the requirements of B cell contact with TH cells? | show 🗑
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| show | 1) Contain no peptides- lipolysaccharides and polysaccarides
2) Only stimulate IgM
3) Create no memory
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| show | By directly stimulating B cells
May act as B-cell mitogens (which activate clones of B cells and are used to assess lymphocytes function)
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| show | dictate the effector function
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| show | TH2
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| If an AB is digested with papain, where does cleavage occur? | show 🗑
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| show | 2 Fab fragments
1 Fc fragment
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| show | One large F(ab2 fragment
Digested Fc frafments
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| What is the function of Fab? | show 🗑
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| show | Binding and bridging
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| Which is bridging of antigens by Abs important? | show 🗑
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| What is the first isotype of Ig that can be produced by a B cell? | show 🗑
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| show | Pentamer
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| show | A J chain
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| show | 10
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| What is the function of IgM? | show 🗑
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| show | Affinity
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| What is the most effective isotype in activating complement? | show 🗑
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| show | Once it undergoes isotype switching by TH2 cells
Because excised DNA is degraded
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| IgM is used as a measure of: | show 🗑
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| Convalescent serum will contain mostly, which immunoglobulin? | show 🗑
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| show | Clones of proliferating antigen-specific B cells
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| show | Single point mutations in the antibody idiotype
If these mutations give them higher affinity, these cells are at an advantage
Clones with higher affinity will predominate
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| show | Clonal selection
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| show | Affinity maturation
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| show | decreases
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| show | GAMDE
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| show | Deficiency of IgA, G, and E and ellevated M
X-linked recessive
Fail to make germinal centers
Susceptible to Pneumocystis carinii infection
Defect in gene coding CD40 L
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| What is the major antibody after IgM? | show 🗑
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| How many subtypes does IgG have? | show 🗑
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| What is the function of IgG? | show 🗑
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| show | IgG
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| show | In the submucosa rather than in the lymph and spleen
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| show | Dimer with a J chain
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| show | Inhibits binding of adhesive substances to mucosal surface
Important component of breast milk
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| show | Mast cells
Basophils
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| show | Immediate type 1 allergic reactions
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| IgE protects against which foreign bodies? | show 🗑
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| Clinical manifestation of immunodeficiencies involving B lymphocytes: | show 🗑
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| Which antibodies act in complement activation? | show 🗑
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| show | IgM and IgD
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| What Abs are on the memory B-cell antigen receptor? | show 🗑
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| What are the functions of the complement system? | show 🗑
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| What is the more primitive pathway of the two complement system activation pathways? | show 🗑
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| show | surfaces of pathogens
C3b + Bb (C3 convertase) --> C3bBb3b(C5 convertase) --> C5b *MAC)
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| The classical pathway is activated by: | show 🗑
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| show | C1, C3, and C5
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| Clinical manifestations of complement deficiencies: | show 🗑
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| show | Which of the following is the most likely Ab preparation?
A) Monoclonal anti-CD-19 IgG
B) MC anti-CD56 IgG
C) Papain treated anti-CD19 IgG
D) Papain anti CD56 IgG
E) Pepsin treated anti-CD19 IgG
F) Pepsin anti-CD56 IgG
Answer: C
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| show | A) Agglutinated
B) Lysed
C) Phagocytosed
D) Precipitated
E) Unaffected - if papain is used
Answer: A
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| A 26 year old obstretic patient becomes ill during the first trimester of pregnancy with fever and lymphadenopathy. Rising titer of anti-Toxoplasma gondii Abs. Full term baby delivered with no apparent signs of utero infection. | show 🗑
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| 4 year old boy is evaluated for possible immunologic deficiency. He has suffered repeated infections of mucosal surface pathogens. Delayed development of protective responses to the standard childhood vaccination. | show 🗑
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| 56 year old homeless, alcoholic, febrile man. Brought to ER after coughing all night. On arrival his pulse is rapid, breathing is labored, Endotracheal aspirates produce a mucopurulent discharge containing gram +ve cocci in chains. Serum high in IgM Abs | show 🗑
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| show | Serum levels of some components of complement are depressed. Which of the following deficiencies could explain his problem?
A) C1
B) C2
C) C3
D) C4
E) C5
Answer: C
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| the cell mediated arm of the immune response (CMI) are designed to kill what pathogens? | show 🗑
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| TH1 cells stimulate which cells? | show 🗑
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| How is TH1 function measured? | show 🗑
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| show | Deficiency of CD8
Ab responses may be higher than usual because of absence of inhibitory responses (IFN-y)
🗑
|
||||
| CTL stimulation requires: | show 🗑
|
||||
| show | 1) Attachment by TCR, CD8, and LFA-1
2) Activation
3) Exocytosis
4) Detachment
🗑
|
||||
| show | 1) Perforins
2) Cytokines
3) Granzymes
4) Fas/FasL
🗑
|
||||
| Function of NK cells: | show 🗑
|
||||
| NK cells are enhanced by: | show 🗑
|
||||
| NK cells are inhibited by: | show 🗑
|
||||
| show | CD16 and CD56
🗑
|
||||
| show | 1) NK cells
2) Macrophages and monocytes
3) Neutrophils
4) Eosinophils
🗑
|
||||
| NK cells recognize their targets via which Ab? | show 🗑
|
||||
| show | Lytic enzymes
TNF
Perforin
🗑
|
||||
| show | TCR
CD3
CD8
CD2
🗑
|
||||
| show | CD16
CD56
CD2
🗑
|
||||
| show | CD14
🗑
|
||||
| show | Perforin
Granzymes
Cytokine (TNF-B. IFN-y)
🗑
|
||||
| Effecotr molecules of macrophages: | show 🗑
|
||||
| show | Block host cell protein synthesis, specifically MHC class 1 synthesis, transport, and expression
However the second CMI response is NK kiling
Exception to this rule is CMV
🗑
|
||||
| 62 year old accountant develops a solid tumor that is unresponsive to chemotherapy. Participates in experiment to stimulate his own immune effector cells to recognize and kill the malignant cells. Tumor cells have no expession of MHC class 1 antigens. | show 🗑
|
||||
| show | transported into the ER and loaded onto MHC molecules that have:
A) a B2 domain instead of a B2 microglobulin
B) Invariant chains
C) Peptide-binding groove
D) Single transmembrane domain
E) Two similar chains
Answer: D (MHC 1)
🗑
|
||||
| show | A) Depressed immune surveillance of tumors
B) Depressed oxygen dependent killing by neutrophils
C) Depressed primary response to soluble antigens
D) Increased cellularity of lymph node paracortical areas
E) Increased tendency to atopy
Answer:A
🗑
|
||||
| 42 year old Nigerian man in the US comes into the hospital clinic. Complains of several months of weight loss, night sweats, mild sputum production, and hemoptysis. You run a PPD skin test and the rests are +ve | show 🗑
|
||||
| Immunologic memory is generated when? | show 🗑
|
||||
| show | IgG, IgA, or IgE
🗑
|
||||
| Function of Activation induced cell death: | show 🗑
|
||||
| Memory cells return to the tissue where: | show 🗑
|
||||
| Effector cells tend to return to areas of: | show 🗑
|
||||
| show | Primary - 5-10 days
Secondary-1-3 days
🗑
|
||||
| show | Primary- IgM, then IgG
Secondary - IgG, IgA, or IgE
🗑
|
||||
| show | Primary: Variable to low
Secondary - High
🗑
|
||||
| show | Primary- All immunogens
Secondary- proteins antigens
🗑
|
||||
| Immunization protocol of responses: | show 🗑
|
||||
| show | Mucosal associated lymphoid tissues
The tonsils and Peyer patches
🗑
|
||||
| show | Transepithelial transport
Protection from proteolytic cleavage
🗑
|
||||
| show | Polyimmunoglobulin receptor
🗑
|
||||
| A patient is suffering from lymphadenopathy and splenomegaly. He has increased lymphocytes, less platelets, and autoimmune anemia. When his peripheral blood leukocytes are exposed to T cell mitogens, they proliferate wildly for weeks. | show 🗑
|
||||
| show | What is the major immunoglobulin produced by the MALT?
A) Dimeric Ig with secretory component
B) Monomeric Ig crosses the placenta
C) Monomeric Ig bound by mast cells
D) Monomeric Ig that opsonizes
E) Pentameric Ig activates complement
Answer: A
🗑
|
||||
| In a lifetime, a person may recieve a dozen or more tetanus toxoid inoculations. When boosters are administered at 10 year intervals, which of the following would be true of the B lymphocytes that respond? | show 🗑
|
||||
| 64 year old man undergoes surgery to excise 18 inches of bowel with adenocarcinoma. When the tissue is examined, the Peyer patches are noted to be hyperplastic with IgA-secreting plasma cell, but there is no secretory IgA in the lumen of the colon. | show 🗑
|
||||
| Immunologic lab is studying migration patterns of different lymphocytes subpopulations. One population of small nondividing lymphocytes which are CD3 and CD4 and express low IL-2 levels, but high levels of LFA-1, labeled with radioactive marker. | show 🗑
|
||||
| show | Passive means - Placental IgG transport/colostrum
Active means- Recovery from infection
🗑
|
||||
| What are the risks of passive immunotherapy? | show 🗑
|
||||
| show | Even attenuated live viruses could cause significant pathology in these individuals
🗑
|
||||
| Clinical importance of natural and passive immunity: | show 🗑
|
||||
| Haemophilus influenza type B vaccine is dependent on: | show 🗑
|
||||
| Living viral vaccines elicit which immune responses? | show 🗑
|
||||
| Killed viral vaccines elicit which immune response? | show 🗑
|
||||
| Hepatitis B vaccine is what type of vaccine? | show 🗑
|
||||
| Experimental vaccine strategies: | show 🗑
|
||||
| show | Passive means - Horse antivenin against black widow spider and snake bite
Horse antitoxin against botulism, diptheria Pooled humman Ig versus Hep A and B, measles, rabies, or tetanus
Active means -Vaccines
🗑
|
||||
| show | Substances that increase the immunogenicity of an antigen when administered with it
🗑
|
||||
| show | 1) Prolonging antigen persistance AlKSO4
2) Enhancing costimulatory signals-muramyl dipeptide
3) Inducing granuloma formation - alum
4) Inducing nonspecific lymphocyte proliferation -LPS
🗑
|
||||
| show | A) Anti-allotype Abs
B) Anti-epitope Abs
C) Anti- idiotype Abs
D) Anti-isotype Abs
E) Anti-rabies Abs
Answer: A
🗑
|
||||
| show | A) Adaptive
B) Artificial active
C) Artificial passive
D) Natural active
E) Natural passive
Answer: B
🗑
|
||||
| A sanitation worker is struck by a car and his leg is crushed against his sanitation truck. The trauma necessitates amputation above the knee. Although the man took a tetanus booster 6 years ago, he was revaccinated. Human pooled , anti-tetanus Ig | show 🗑
|
||||
| 28 year old man brought into court for not paying child support. 20 year old insists he is the father. the court suggests before the hearing that genetic tests are performed on the mother, father and child. One of the tests was for genetic Ig | show 🗑
|
||||
| In 1988, a new childhood vaccine was developed to protect against epidemic meningitis by mixing HIB polysaccharide with whole, killed Bordatella Pertussis bacteria. | show 🗑
|
||||
| show | Defect - Deficiency of NADPH oxidase/failure to generate O2 radicals
Symptoms - Recurrent infections with catalase positive bacteria and fungi
🗑
|
||||
| Molecular defects and symptoms of Chediak Higashi syndrome: | show 🗑
|
||||
| show | Defects: Deficiency of essential enzyme in hexose monophosphate shunt
Symptoms-Same as CGD, with associated anemia
🗑
|
||||
| Molecular defects and symptoms of Myeloperoxidase deficiency: | show 🗑
|
||||
| show | Defect- Absence of CD18
Symptoms- Recurrent and chronic infections
Fail to form pus
Do not reject umbilical cord stump
🗑
|
||||
| What are the defects of phagocytic cells? | show 🗑
|
||||
| show | 1) Bruton X-linked hypogammaglobulinemia
2) Transient hypogammaglobulinemia of infancy
3) Common variable hypogammaglobulinemia
4) Selective IgA deficiency
5) X-linked hyper IgM syndrome
🗑
|
||||
| show | Deficiency of tyrosine kinase blocks B-cell maturation
🗑
|
||||
| show | Low Igs of all classes
No circulating B cells
Pre-B cells in bone marrow
🗑
|
||||
| show | Monthly gamma-globulin replacement
Abs for infection
🗑
|
||||
| Molecular defect of transient hyogammaglobulinemia of infancy: | show 🗑
|
||||
| show | Detected in 5th to 6th month of life
Resolves by 16-30 months
Susceptibility to pyogenic bacteria
🗑
|
||||
| show | Antibiotics
Gamma-globulin replacement
🗑
|
||||
| show | Unknown
🗑
|
||||
| Symptoms/signs of common variable hyogammaglobulinemia: | show 🗑
|
||||
| show | Antibiotics
🗑
|
||||
| Molecular defect of selective IgA deficiency: | show 🗑
|
||||
| Symptoms/signs of selective IgA deficiency: | show 🗑
|
||||
| show | Antibiotics, not Igs
🗑
|
||||
| Molecular defect of X-linked hyper IgM syndrome: | show 🗑
|
||||
| Symptoms/signs of X-linked hyper IgM syndrome: | show 🗑
|
||||
| Treatment of X-linked hyper IgM syndrome: | show 🗑
|
||||
| Deficiencies in the classical pathway occur where? | show 🗑
|
||||
| Signs/diagnosis of classic pathway deficiency: | show 🗑
|
||||
| show | Factor B, properdin
🗑
|
||||
| Signs/diagnosis of alternative pathway deficiency: | show 🗑
|
||||
| show | C3
C5, C6, C7, and C8
🗑
|
||||
| Signs/diagnosis of C3 deficiency: | show 🗑
|
||||
| show | Reccurent meningococcal and gonococcal infections
🗑
|
||||
| Deficiencies in complement regulatory proteins occur where? | show 🗑
|
||||
| show | Overuse of C1, C4, or C2
Edema at mucosal surfaces
🗑
|
||||
| show | Paroxysmal nocturnal hemoglobinuria
🗑
|
||||
| Diseases of selective T cell deficiency: | show 🗑
|
||||
| show | Failure of formation of the 3rd and 4th pharyngeal pouches
Thymic aplasia
🗑
|
||||
| show | Facial abnormalities
Hypoparathyroidism
Cardiac malformations
Depression of T cell numbers
Absence of T cell responses
🗑
|
||||
| What is the defect in MHC class 1 deficiency? | show 🗑
|
||||
| show | CD8 T cells deficient
CD4 cells normal
Recurring viral infections
Normal DTH and Ab
🗑
|
||||
| What are the diseases of combined partial B and T cell deficiency? | show 🗑
|
||||
| Defect in Wiskott Aldrich syndrome: | show 🗑
|
||||
| show | Defective responses to bacterial polysaccharides
Depressed IgM
Gradual loss of CMI and HMI
Thrombocytopenia
Eczema
🗑
|
||||
| show | Defect in kinase involved in the cell cycle
🗑
|
||||
| Clinical manifestations of Ataxia telangiectasia: | show 🗑
|
||||
| What are the diseases of complete functional B- and T-cell deficiency? | show 🗑
|
||||
| show | 1) Defects in common y chain of IL-2 receptors (present in receptors for il-4,-7,-9,-15) -- X linked
2) Adenosine deaminase deficiency
3) Defect in signal transduction from T-cell IL-2 receptors
4) Bare lymphocytes syndrome
🗑
|
||||
| show | Chronic Diarrhea
Skin, mouth, and throat lesions
Opportunistic fungal infections
Low levels of irculating lymphocytes
Cells unresponsive to mitogens
🗑
|
||||
| show | T cells present and responsive to non-specific mitogens
No GVHD
Deficient in CD4
Hypogammaglobulinemia
🗑
|
||||
| show | A) Antibody dependent cell mediated cytotoxicity of parasite agents
B) Cellularity of splenic PALS
C) Cytotoxic killing of virus infected targets
D) Generation of oxygen metabolites
E) Proliferative response to concavalin A
Answer: D
🗑
|
||||
| 14 month old male infant is reffered to a specilaist for diagnosis of an immunologic deficiency. For 4 months the child has suffered repeat bacterial infections and pneumoncoccal vaccine has failed. Absence of cells responsive to pokeweed mitogen. | show 🗑
|
||||
| 31 year old man treated for 4th episode of disseminated Neisseria gonnorhea infection in the last 5 years. He had no previous history of unusual or recurrent infection. If he has an immunologic defect, which of the following is most likely? | show 🗑
|
||||
| A patient has been hospitalized 3 times for painful abdominal edema and is now complaining of swollen lips. What will lab findings in this patients most likely include? | show 🗑
|
||||
| 4 year old girl presents with sever Staph aureus abcess. Her history is significant for a previous Serratia marcasens infection. If she has an enzyme deficiency, which of the following is most likely? | show 🗑
|
||||
| show | No eczema or bleeding problems. Which disease is indicated by these findings?
A) Bruton X-linked agammablobilunemia
B) CGD
C) DiGeorge syndrome
D) SCID
E) Wiskott-Aldrich syndrome
Answer: B (Negative NBT --> no oxygen radicals)
🗑
|
||||
| Acutely ill 2 year old boy hospitalized with Staph aureus pneumonia, which is treated appropriately. Recovered from measles 6 months ago. Scant tonsillar tissue and no palpable lymphadenopathy. Electrophoresis reveals subnormal levels of y-globulins. | show 🗑
|
||||
| show | What lab finding would support this suspicion?
A) Depressed C3
B) Depressed C4
C) Depressed C5
D) Elevated C1
E) Elevated C1,4, and 2
Answer: B
🗑
|
||||
| HIV infects which cells? | show 🗑
|
||||
| The HIV virus uses which chemokine receptors as coreceptors? | show 🗑
|
||||
| Mechanisms by which HIV destroys the Immune system: | show 🗑
|
||||
| How does multiplication in lymphovytes and macrophages affect the immune system? | show 🗑
|
||||
| show | Eliminates cell and antibody mediated immunity
🗑
|
||||
| show | Makes infected cells less susceptible to CTL killing
🗑
|
||||
| show | Inhibits cytokine synthesis in both infected and uninfected cells
🗑
|
||||
| Destruction of TH cells by HIV leads to: | show 🗑
|
||||
| What is the immunologic result of deviation towards the TH2 response? | show 🗑
|
||||
| What effect does antigenic drift and heavy glycosylation of gp120 have on the immune system? | show 🗑
|
||||
| Which cells serve as the reservoirs for HIV infection? | show 🗑
|
||||
| show | There is an initial, massive response by CD8 cells which controls the viremia and transition into clinical latency, but these leads to the death of many CD4 cells (which amplify the cytoxic response), so the amplification loop for CTL stimulation will end
🗑
|
||||
| How can HIV be diagnosed? | show 🗑
|
||||
| show | How should this patient be counseled?
A) She and her baby are both infected with HIV
B) She is -ve for HIV because RPR is more specific
C) She is positive for HIV
D) She should have a PCR performed
E) False-positive HIV result
Answer: D
🗑
|
||||
| A neonate born to an HIV-positive mother is evaluated for HIV. What would be the assay of choice? | show 🗑
|
||||
| Attachment of HIV to TH is initiated by binding of HIV gp120 to CDR receptor. Then gp120 undergoes a conformational change and binds to a second molecule. What is the second molecule on the surface of CD4 that acts as coreceptor & binds lymphotropic HIV? | show 🗑
|
||||
| Male exotic dancer has been HIV positive for 10 years. Because of his low income, he can only irregularly afford the anti-retroviral drugs prescribed to him. When he goes for a checkup, his CD count is 390/mm^3, Which immunologic parameter is most | show 🗑
|
||||
| show | A) IFN-y
B) IL-1
C) Il-2
D) IL-10
E)TNF-B
Answer: D
🗑
|
||||
| show | 1) Excessive responses to foreign antigens
2) Autoimmunity (failure of self tolerance)
🗑
|
||||
| What are the types of hypersensitivity? | show 🗑
|
||||
| show | IgE
🗑
|
||||
| show | Mast cells and their mediators
🗑
|
||||
| show | IgM, IgG Abs against cell or tissue
Ags
🗑
|
||||
| What is the mechanism of tissue injury in type 2 hypersensitivity? | show 🗑
|
||||
| What is the immune mechanism in Immune-complex mediated/Type 3 hypersensitivity? | show 🗑
|
||||
| What is the mechanism of tissue injury in type 3 hypersensitivity? | show 🗑
|
||||
| show | 1) CD4 T cells (delayed type)
2) CD CTLs (T-cell mediated cytolysis)
🗑
|
||||
| show | Macriophage activation
Cytokine mediated inflammation
🗑
|
||||
| show | Direct target cell killing
Cytokine mediated inflammation
🗑
|
||||
| show | 1) The fist exposure to the antigen sensitizes lymphocytes
2) Subsequent exposure elicit damage
3) Response is Ag-specific
🗑
|
||||
| Characteristics of Type 1 hypersensitivity: | show 🗑
|
||||
| What are the type 1 effector cells? | show 🗑
|
||||
| Two to four hours after the immediate response to release of these mediators, what reaction begins? | show 🗑
|
||||
| show | 1) Histamine -Smooth muscle contraction
2) Heparin - anticoagulant
3) Eosinophils -chemotaxis
🗑
|
||||
| show | 1) PE2- Increased pain and vascular permability
2) PD2- Smooth muscle contraction and VP
3) Leukotrienes C4,D4,E4- Smooth muscle contraction and VP
4)Leukotriene B4- chemotactic for neutrophils
🗑
|
||||
| What are the different types of allergic diseases? | show 🗑
|
||||
| show | Trees, grass, dust, cats, dogs, mites
🗑
|
||||
| What are the possible allergens in food allergies? | show 🗑
|
||||
| show | Insect stings
Used in vivo skin testing for allergies
🗑
|
||||
| show | Inhaled materials
🗑
|
||||
| show | Insect stings, snake venoms, drug reactions
🗑
|
||||
| Clinical finding in allergic rhinitis: | show 🗑
|
||||
| Clinical finding in food allergies: | show 🗑
|
||||
| show | Local skin
Edema
Reddening
Vasodilation
🗑
|
||||
| show | Bronchial and tracheal constriction
Edema
Mucus production
Massive inflammation
🗑
|
||||
| show | Bronchial and tracheal constriction
Complete vasodilation and death
🗑
|
||||
| In type 2 hypersensitivity, the Abs produced cause damage by: | show 🗑
|
||||
| show | 1) Autoimmune hemolytic anemia
2) Autoimmune thrombocytopenic purpura
3) Goodpasture
4) Acute rheumatic fever
5) Myasthenia gravis
6) Graves
7) Type 2 diabates
8) Pernicious anemia
🗑
|
||||
| show | RBC membrane proteins (Rh, Ags)
🗑
|
||||
| Target antigen of autoimmune thrombocytopenia purpura: | show 🗑
|
||||
| Target antigen of Goodpasture antigen: | show 🗑
|
||||
| show | Streptococcal cell-wall Ag
Ab cross-reacts with myocardial Ag
🗑
|
||||
| show | Acethylcholine
🗑
|
||||
| Targert antigens of graves disease: | show 🗑
|
||||
| show | Insulin receptors
🗑
|
||||
| Target antigens of pernicious anemia: | show 🗑
|
||||
| What is the mechanism of pathogenesis of autoimmune hemolytic anemia? | show 🗑
|
||||
| What is the mechanism of pathogenesis of autoimmune thrombocytopenic purpura? | show 🗑
|
||||
| What is the mechanism of pathogenesis of goodpasture syndrome? | show 🗑
|
||||
| What is the mechanism of pathogenesis of acute rheumatic fever? | show 🗑
|
||||
| show | Ab inhibits Ach binding
Down modulates receptors
🗑
|
||||
| What is the mechanism of pathogenesis of Graves disease? | show 🗑
|
||||
| show | Ab inhibits binding of insulin
🗑
|
||||
| show | Neutralization of intrinsic factor
Decreased absorption of vitamin B12
🗑
|
||||
| show | Hemolysis
Anemia
🗑
|
||||
| Clinical manifestation of autoimmune thrombocytopenic purpura: | show 🗑
|
||||
| show | Nephritis
Lung Hemmorhage
🗑
|
||||
| show | Myocarditis
Arthritis
🗑
|
||||
| Clinical manifestations of myasthenia gravis: | show 🗑
|
||||
| show | Hyperthyroidism followed by hypothyroidism
🗑
|
||||
| show | Hyperglycemia
Ketoacidosis
🗑
|
||||
| Clinical manifestations of pernicious anemia: | show 🗑
|
||||
| show | Erythroblastosis fetalis
🗑
|
||||
| Erythroblastosis fetalis is what type of hypersensitivity? | show 🗑
|
||||
| If a mother is Rh-, and the father is Rh+, what will happen? | show 🗑
|
||||
| show | Treating the mother with RhoGam (a preparation of human anti-RhD igD Ab) at 28 weeks of gestation and within 72 hours after birth
🗑
|
||||
| Characteristics of Type 3 hypersensitivities: | show 🗑
|
||||
| Examples of diseases of Type 3 hypersensitivity: | show 🗑
|
||||
| Antigens involved in SLE: | show 🗑
|
||||
| show | IgM versus IgG Fc region
🗑
|
||||
| Antigens involved in poststreptococcal glomerulonephritis: | show 🗑
|
||||
| show | Various proteins
🗑
|
||||
| Antigens involved in arthus reaction: | show 🗑
|
||||
| show | Nephritis
Arhtitis
Vasculitis
Rash
🗑
|
||||
| show | Joint pain
Erosions
🗑
|
||||
| Clinical manifestations of postsreptococcal glomerulonephritis: | show 🗑
|
||||
| show | Arthritis
Vasculitis
Nephritis
🗑
|
||||
| Clinical manifestations of arthus reaction: | show 🗑
|
||||
| Characteristics of Type 4/T-cell mediated hypersensitivites: | show 🗑
|
||||
| show | 1) Type 1 diabetes
2) Multiple sclerosis
3) Contact dermatitis
4) Peripheral neuritis
5) Guillain Barre syndrome
6) Hashimotos thyroiditis
🗑
|
||||
| Specificity of pathogenic T cells in Type 1 DM: | show 🗑
|
||||
| Specificity of pathogenic T cells in Multiple sclerosis: | show 🗑
|
||||
| show | Nickel
Poison Ivy/oak catechols
Hapten/carrier
🗑
|
||||
| Specificity of pathogenic T cells in Peripheral neuritis: | show 🗑
|
||||
| show | Peripheral nerve myelin or gangliosides
🗑
|
||||
| show | Unknown Ag in thyroid
🗑
|
||||
| Clinical manifestations of Type 1 DM: | show 🗑
|
||||
| Clinical manifestations of Multiple sclerosis: | show 🗑
|
||||
| Clinical manifestations of contact dermatitis: | show 🗑
|
||||
| Clinical manifestations of peripheral neuritis: | show 🗑
|
||||
| show | Ascending paralysis
Peripheral nerve
Demyelination
🗑
|
||||
| show | Hypothyroidism
🗑
|
||||
| Effector cells of each hypersensitivity reaction: | show 🗑
|
||||
| show | Myasthenia gravis
Graves disease
Type 2 DM
🗑
|
||||
| show | Type 4
🗑
|
||||
| show | Type 2 cytotoxic
Type 3
🗑
|
||||
| show | Type 4
🗑
|
||||
| show | Failure of self tolerance
The strongest genetic associations with the development of autoimmune diseases are the class 2 MHC genes
Environment associations -infections
Hormones
🗑
|
||||
| Infections can trigger autoimmunity through: | show 🗑
|
||||
| Therapies for immune diseases: | show 🗑
|
||||
| show | 1) Desensitization by injecting small doses od allergens
2) Plasmapheresis
3) High doses of IV IgG- may bind to Fc receptors and inibit synthesis
4) Tolerance induction - high dose administration of antigens
🗑
|
||||
| show | An examination of the fluid should reveal what?
A) Activated L lymphocytes
B) Abs against type 4 collagen
C) Abs against double stranded DNA
D) Abs against microsomal Ags
E) IgM Abs reactive with the Fc region of IgG
Answer:E
🗑
|
||||
| show | A) y-INF
B) IL-2
C) IL-3
D) IL-8
E) IL-10
Answer:E
🗑
|
||||
| In individuals exposed to massive doses of cercariae, IgG Abs developed in response to the developing worms and when the adults release eggs, the patients suffer acute and life threatening symptoms of fever, edema, arthralgia, and rash | show 🗑
|
||||
| show | A) Her husband should be tested for Rh incompatibility
B) She is RhD- and should be treated with Rhogam
C) She is RhD-, no risk to a fetus
D) She is RhD+ and should be treated with Rhogam
E) She is RhD+, no risk to the fetus
Answer: E
🗑
|
||||
| On first ecposre, cercariae penetrate the skin and become schistomula, which enter the circulation and eventually mature in the mesentric veins. On subsequent exposure, schistosomula are frequently killed within minutes by an immune response in the skin. | show 🗑
|
||||
| show | Tissues taken from donor given to the host
🗑
|
||||
| show | Transfusion
🗑
|
||||
| show | 1) Autografts - same individual
2) Syngeneic grafts - genetic individuals
3) Allogenis grafts- genetically different members of same species
4) Xenogeneic grafts- different species
🗑
|
||||
| MHC alleles are expressed: | show 🗑
|
||||
| What are the effectors of Graft rejection? | show 🗑
|
||||
| show | 1) Hyperacute
2) Accelerated
3) Acute
4) Chronic
🗑
|
||||
| show | Hyperacute - minutes to hours
Accelerated - days
Acute - days to weeks
Chronic-months to years
🗑
|
||||
| show | Preformed anti-donor Abs and complement
🗑
|
||||
| Cause of accelerated graft rejection: | show 🗑
|
||||
| Causes of acute graft rejection: | show 🗑
|
||||
| Causes of chronic graft rejection: | show 🗑
|
||||
| Characteristics of Graft-Versus-Host disease: | show 🗑
|
||||
| show | ABO blood typing
HLA matching
Screening for Abs
Crossmatching
Mixed Lymphocyte reaction -type 2
Microcytotoxicity test- class 1
🗑
|
||||
| How is ABO blood typing used to test tissue compatibility? | show 🗑
|
||||
| show | match the HLA antigens of recipient and donor
The larger number of matched MHC allele, the better the graft survival
🗑
|
||||
| show | HLA-A, HLA-B, and HLA-DR
🗑
|
||||
| show | Use microcytotoxicity test
🗑
|
||||
| show | Use mixed lymphocyte reaction (MLR)
Lymphocytes are irradiated so they can't proliferate, but act as stimulator cells for presenting MHC antigens
If the antigens are the same, no proliferation will occur
🗑
|
||||
| Characteristics of immunosupression: | show 🗑
|
||||
| What does generalized immunosupression do? | show 🗑
|
||||
| What therapies are used to prevent graft rejection? | show 🗑
|
||||
| show | Cyclophosphamide
Methotrexate
🗑
|
||||
| show | Prednisone
Dexamethasone
🗑
|
||||
| What drugs are fungal metabolites? | show 🗑
|
||||
| show | Anti-CD3
Anti-IL2 receptor
Anti-CD40L
🗑
|
||||
| Action and use of mitotic inhibitors? | show 🗑
|
||||
| Action and use of corticosteroids? | show 🗑
|
||||
| Action and use of fungal metabolites? | show 🗑
|
||||
| Actions and use of experimental monoclonals? | show 🗑
|
||||
| show | A) Allograft
B) Autograft
C) Heterograft
D) Syngeneic graft
E) Xenograft
Answer:D
🗑
|
||||
| show | and bloody diarrhea appear.10 months after- the patient dies. Which effector mechanism is most closely associated with this rejection reaction?
A) Macrophages
B) Abs and complement
C) CD8
D) LAK cells
E) NK cells
Answer: C
🗑
|
||||
| show | A) Corticosteroids, such as prednisone for life
B) Fungal metabolites, such as cyclosporin A, for life
C) Mitotic inhibitors, such as cyclophosphamide for life
D) Monoclonal anti-IL2 receptor for life
E) No treatment required
Answer: E
🗑
|
||||
| What are the immunopriveledged areas in the human being? | show 🗑
|
||||
| In heart lung transplants, where the critical illness of the recipient and his inability to preserve tissue from brain dead donor often precludes tissue typing. In one immunosupressive experiment, patients are treated with anti-CD28Ab Fab fragments | show 🗑
|
||||
| Tumor antigens: | show 🗑
|
||||
| show | CTLs
Antibodies (with complement of ADCC)
Macrophages
NK cells
🗑
|
||||
| How do tumors evade the immune system? | show 🗑
|
||||
| show | 1) Vaccination
2) Increase costimulatory moleciles
3) Stimulate T cell proliferation and differentiation
4) Antitumor Abs
5) Immunotoxins
6) Administrate tumor reactive T and NK cells from culture
🗑
|
||||
| show | HIB
🗑
|
||||
| show | Induce increases in MHC 1 and 2 expression
Increase the efficiency of APCs to CTL and TH cells
🗑
|
||||
| show | Treatment of hepatitis B and C
Treatment of hairy B-cell leukemia, CML, and Kaposi sarcoma
Multiple sclerosis
CGD
🗑
|
||||
| show | Ag excess: early infection
Equivalence: window period
Ab excess: late
🗑
|
||||
| show | Direct-Abs bound to RBC
Indirect- production of anti RBC antibodies
🗑
|
||||
| show | Detect and localize Ags in tissue via binding of flourescent Abs
Used to diagnose RSV, Herpes simplex 1 and 2, and pneumocystis infections
🗑
|
||||
| show | pathogen specific Abs
Anti-Ig is added, if binding occur
Used to detect antinuclear Abs, Anti-ds DNA ab, anti-thyroid Abs, antiglomerular Abs, and anti-EBV Ag Abs
🗑
|
||||
| show | Extremely sensitive tests
Used to detect the presence of hormones, drugs, Anti-biotics, serum proteins, Ags, and tumor markers.
RIA- uses radiolabeled product
ELISA- presence of enzyme mediated color change
🗑
|
||||
| In the screening fro HIV, which test is used? | show 🗑
|
||||
| What test is used as a confirmation of HIV? | show 🗑
|
||||
| show | Viral organism--> proteins
Proteins seperated SDS PAGE
Proteins transferred onto nitrocellulose sheet
Reacted with patient serum
Antihuman y globulin labeled and reacted for color development/identifation
Cells with high flourescne--> top right
🗑
|
||||
| When do we use flow cytometry to analyze cell populations? | show 🗑
|
||||
| Acts at three sites: antigen recognition site, proliferation step, and differentiation/synthesis steps: | show 🗑
|
||||
| show | proliferation; differentiation/synthesis sites
🗑
|
||||
| show | prednisone (Deltasone)
🗑
|
||||
| show | prednisone (Deltasone)
Tacrolimus
Azathioprine (Imuran)
dactinomycin (Cosmegen)
methotrexate
cyclophosphamide (Cytoxan)
🗑
|
||||
| dactinomycin (Cosmegen) also inhibits which steP/ | show 🗑
|
||||
| Which agents have an Anti-profilerative site of action: | show 🗑
|
||||
| show | antigen recognition site
🗑
|
||||
| show | Prednisone(Deltasone)
🗑
|
||||
| show | inhibition of leukotriene production
inhibition of prostaglandins
🗑
|
||||
| Effective in lowering incidents of rejection in infectious complications in transplant patients: | show 🗑
|
||||
| Tests of immunocompetency:-- measurements | show 🗑
|
||||
| show | cyclosporine (Sandimmune, Neoral)
🗑
|
||||
| show | tacrolimus (FK 506)
🗑
|
||||
| Implicated in initiation of hypersensitivity vasculitis; a Type III vasculitic reaction: | show 🗑
|
||||
| Blockade of mediator release following exposure of sensitized tissue mast cells or blood basophils to drugs that initiate Type I drug allergic reactions: | show 🗑
|
||||
| show | IFN-a
🗑
|
||||
| What is levamisole? | show 🗑
|
||||
| For synthesized for treating parasitic infections, this drug is now FDA approved for clinical use in the treatment of Dukes class C colorectal cancer after surgery: | show 🗑
|
||||
| Alkylating agent; destroys proliferating lymphoid cells; in low doses -- for effective against autoimmune disorders including systemic lupus erythematosus | show 🗑
|
||||
| show | azathioprine (Imuran)
🗑
|
||||
| show | Methotrexate
🗑
|
||||
| show | Cyclophosphamide (Cytoxan)
vincristine (Oncovin)
methotrexate
cytarabine (ARA-C)
🗑
|
||||
| Congenitally-acquired immunodeficiency disease | show 🗑
|
||||
| adenosine deaminase deficiency | show 🗑
|
||||
| strong tropism for CD4+ helper T cells | show 🗑
|
||||
| reaction effective in eliminating infections caused by intracellular pathogens (e.g. Leishmania) | show 🗑
|
||||
| show | activated cytotoxic T cell
🗑
|
||||
| activated lymphocytes | show 🗑
|
||||
| show | effectors of humoral immunity
🗑
|
||||
| IL-4, IL-5, IL-6 produced by this subset of T cells | show 🗑
|
||||
| show | Class I MHC molecules
🗑
|
||||
| show | Class II MHC molecules
🗑
|
||||
| Immediate hypersensitivity type associated with hemolytic disease in the newborn | show 🗑
|
||||
| show | Type I hypersensitivity
🗑
|
||||
| show | interferon alpha-2a
🗑
|
||||
| HypRho-D | show 🗑
|
||||
| Atgam | show 🗑
|
||||
| Most important anatomical sites for mast cells distribution and IgE sensitization: | show 🗑
|
||||
| show | prednisone;
alternatives -- mercaptopurine, cyclophosphamide
🗑
|
||||
| show | cyclophosphamide plus factor XIII
🗑
|
||||
| Idiopathic thrombocytopenic purpura: treatment drug of choice | show 🗑
|
||||
| show | Rho D immune globulin
🗑
|
||||
| show | histamine, leukotrienes, kinins, prostaglandins, serotonin, platelet-activating factor
🗑
|
||||
| show | isoproterenol, theophylline, epinephrine, cromolyn
🗑
|
||||
| Immunomodulator -- FDA approved for use in combination with flurouracil in treatment of Dukes class C colorectal cancer after surgery | show 🗑
|
||||
| show | Either from the Sternum or The iliac crest
🗑
|
||||
| show | azathioprine
🗑
|
||||
| show | thalidomide
🗑
|
||||
| show | prednisone
🗑
|
||||
| show | dexamethasone
🗑
|
||||
| Useful in management of idiopathic thrombocytopenic purpura refractory to prednisone | show 🗑
|
||||
| Drug of choice in treating hemolytic anemia of the newborn: | show 🗑
|
||||
| show | A) cancer treatment
B) multiple sclerosis
🗑
|
||||
| show | A) thymosin
B) interferon beta
C) interferon-gamma
D) TNF alpha
🗑
|
||||
| Inhibits antigen recognition of B-cell | show 🗑
|
||||
| show | bacteria
🗑
|
||||
| show | C-reactive protein, mannose-binding protein, complement factors
🗑
|
||||
| show | Heat shock proteins and MIC (MICA and MICB)
🗑
|
||||
| How many domains are there in different Igs? | show 🗑
|
||||
| show | HYPERVARIABLE REGIONS
🗑
|
||||
| show | CDR1…..[a.a #26] CDR2…..[a.a#53] CDR3[a.a#96]
Most variable one is CDR3
🗑
|
||||
| The light chain can be of two classes : | show 🗑
|
||||
| Which subclass of IgG doesn't cross the placenta? Which subclass doesn't activate the complement? | show 🗑
|
||||
| show | 14
🗑
|
||||
| show | 2
🗑
|
||||
| lambda chain is on | show 🗑
|
||||
| Combinatorial diversity is calcultaed as | show 🗑
|
||||
| Mannose binding protein [mannan lectin ] pathway: | show 🗑
|
||||
| show | Turbidimetry
Nephalometry
These 2 tests are quantitative & qualitative
🗑
|
||||
| Single radial immunodiffusion | show 🗑
|
||||
| show | Quantitative
Expose the reactants to an electrical current
Start at neutral pH
Assign standards
Apply the current, the current will affect the Ags
Make them migrate toward the cathode
Measure the distance travelled by Ags
🗑
|
||||
| show | looking for Abs against Salmonella Typhi Ags in the serum
of the patient
͞Rising Titer: a titer should be increased 4 folds or more to be considered significant
Other infections like Brucellosis
🗑
|
||||
| show | Mix the cells in a liqui-put them through this system
They come out one after the other,hit them with a laser
Scattering of light at (an angle)
The bigger the cell, the less it will scatter light forward
The scattered light indicates granularity
🗑
|
||||
| show | Bring Abs against relevant antigen
Before we mix these Abs we label them
1st one with fluorescein, 2nd one with rhodamine etc
Mix these labeled different Abs with cells in the mixture
wash excess and pass these cells in line like in flow cytometer
🗑
|
||||
| Follicular B-cells "FO-B cells": | show 🗑
|
||||
| show | Undergo some transitional processes; designated as T1- and T2- B cells
Responsible for encountering the Ags which are made of polysaccharids, expressing only IgM on their surface -No Memory Cells
They can give rise to naïve memoryB-cells
🗑
|
||||
| show | B1-cells or CD5 B-cells, because it expresses the CD5 molecule on their surfaces. These cells are apparently produced in the fetus , propagate themselves and continue dividing there
Only IgM
🗑
|
||||
| show | 1) Apoptosis
2) Anergy
3) Receptor Editing: the B-cells, here, is given a chance to reactivate RAG-1 & RAG-2 and try to assemble a different light chain
4) Immunological Ignorance
🗑
|
||||
| Pokeweed mitogen Acts upon | show 🗑
|
||||
| Concanavalin & Phytohaemagglutinin is a plant mitogen, and is known for its ability to stimulate | show 🗑
|
||||
| show | the non-random association of alleles at different
loci
🗑
|
||||
| show | APS (Autoimmune polyendocrinopathy Syndrome )
🗑
|
||||
| show | IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked syndrome)
🗑
|
||||
| Suggested mechanism by which natural autoantibodies “ fight ” bacteria is | show 🗑
|
||||
| show | IgG variety
🗑
|
||||
| show | rheumatic fever
🗑
|
||||
| The conversion of H antigen to A or B antigen is dependent on transferase enzymes : | show 🗑
|
||||
| mutation in fucose transferase because of that they can't add fucose to the terminal part of the H-chain consequently they can't add neither NAGA nor galactose this phenotype is called | show 🗑
|
||||
| show | 5
D, C, E, c and e
🗑
|
||||
| show | absence of the D antigen
🗑
|
||||
| Rhesus antigens are | show 🗑
|
||||
| show | Carbohydrates (sugars), and the antibodies that are produced against them are IgM antibodies
🗑
|
||||
| There are two possible mechanisms of action, in case of Rh immunization: | show 🗑
|
||||
| What is febrile reaction? | show 🗑
|
||||
| What are the symptoms of a faulty transfusion {cross match ABO incompatibility}? | show 🗑
|
||||
| show | will only happen if the recipient has anti HLA Abs, if there are a high number of these anti HLA antibodies, they might activate the complement system in the lungs and lead to pulmonary EDEMA
🗑
|
||||
| The Natural mechanisms for avoiding “FETUS GRAFT REJECTION” are : | show 🗑
|
||||
| Factors that can be deficient are: | show 🗑
|
||||
| C1 inhibitor "C1-INH" | show 🗑
|
||||
| show | CR1 is present on RBC to
remove immune complexes from blood to spleen, so patients are more susceptible to immune complex diseases like SLE
🗑
|
||||
| show | Bruton’s Agammaglobulinemia.
Transient Hypogammaglobulinemia of Infancy.
Selective IgA
- Selective IgG
- X-linked Hyper-IgM
Common variable
Good syndrome
Selective IgM:
🗑
|
||||
| T-cell problems | show 🗑
|
||||
| SCID: | show 🗑
|
||||
| - Selective IgM Deficiency | show 🗑
|
||||
| show | Involves a certain subclass, the most common being the ones affecting IgG2 and IgG3
IgG1 is very rare
IgG4 deficiency is not actually a problem- no symptoms of immunodeficiency
🗑
|
||||
| Cancer antigens: | show 🗑
|
||||
| Carcinogenic viruses: | show 🗑
|
||||
| show | 1-properdin deficiency
2-2/3 chronic granulomatous disease (the rest 1/3 are recessive)
3-Brutonagammaglobulinemia (x-linked recessive)
4-X-linkged hyper IgM syndrome
5-x-linked SCID
6-Wiskott-Aldrich syndrome
🗑
|
||||
| Recessive: | show 🗑
|
||||
| dominant | show 🗑
|
||||
| show | sirolimus
🗑
|
||||
| show | abcimixab
🗑
|
||||
| show | Muromonab
🗑
|
||||
| show | Daclizumab, basiliximab
🗑
|
||||
| show | 1- Decrease the expression of transcription factors (IL-1, IL-2, IL-3, IL-4)
2- Increase transcription of lipocortin, which is an important component in anti-inflammatory
🗑
|
||||
| Clinical uses for steroids: | show 🗑
|
||||
| Side effects of steroids: | show 🗑
|
||||
| Calcineurine inhibitors: | show 🗑
|
||||
| Function of Cyclosporines , Tacrolimus | show 🗑
|
||||
| Uses of calcieurine inhibitors: | show 🗑
|
||||
| show | 1- liver toxicity
2- nephrotoxicity
3-hypertension
4-hyperkakemia
5-hyperglycemia
6- viral infection
7- lymphoma, hirsutism, gum hyperplasia
8- anaphylaxis after IV administration
🗑
|
||||
| both calcineurine inhibitors cause | show 🗑
|
||||
| The predominant enzyme responsible for metabolism of tacrolimus and cyclosporine is | show 🗑
|
||||
| show | Inhibits the CELLULAR IMMUNITY throw inhibiting kinase activity
of mammalian target of rapamycin (mTOR)and decrease the IL activity
🗑
|
||||
| When is sirolimus used? | show 🗑
|
||||
| show | 1) Methotrexate
2) Azathioprine-Micropbenolate is better
Glucocorticoid + Cyclosporine/tacrolimus + Azathioprine
🗑
|
||||
| kidney transplantation surgery, what do you have to do? | show 🗑
|
||||
| show | treatment of acute rejection of renal
allograft as well as for corticosteroid-resistant acute
allograft rejection in cardiac and hepatic transplant
patients
also used to deplete T cells from donor bone
marrow prior to transplantation
🗑
|
||||
| Anti IL-2 | show 🗑
|
||||
| Uses of Basiliximab | show 🗑
|
||||
| show | Infliximab
🗑
|
||||
| Bone marrow rejection: | show 🗑
|
||||
| Atopic asthma: | show 🗑
|
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