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Immunology Exam OSU
The first exam in medical microbiology
| Question | Answer |
|---|---|
| TLR 2 | binds to peptidoglycans of Gram -positive bacteria on cell surface |
| TLR 4 | binds to LPS of Gram -negative bacteria receptor on cell surface |
| TLR 5 | binds to flagella of multiple bacteria on cell surface |
| TLR 9 | binds to bacterial unmethylated cpg DNA and viral DNA (in Lupis found to be important) This is an endosomal receptor |
| TLR 3 | binds to viral dsRNA This is an endosomal receptor |
| TLR 7 and TLR 8 | binds to ss- viral RNA This is an endosomal receptor that detects single stranded viral RNA |
| NOD1 | binds to peptidoglycans from Gram-negative bacteria. This is a cytoplasmic receptor |
| NOD 2 | binds to peptidoglycans from Gram-positive bacteria This is a cytoplasmic receptor |
| RIG-1 | binds to HCV RNA This is a cytoplasmic receptor |
| NOD | nuclear oligomerization domain |
| All of the TLRs... | activate similar signaling pathways on recognition of microbial ligands: Activation of transcription factors result in expression of genes for cytokine /chemokine production |
| NFkB | Cytokine Production, activate adhesion molecules This is part of the signal cascade of Toll-Like receptors. |
| IRF-3 | another molecule in the TLR signaling cascade responsible for Type 1 interferon blocks viral replication |
| TLR-4 can cause? | pathophysiology when are certain polymorphism; activated too often...it is found to be a reason for asthma in children. |
| TLRs are helpful for what... | TLR signaling in B cells promotes auto-antibody production.TLR ligands, such as CpG nucleotides or others are therefore useful adjuvants to enhance effectiveness of vaccines. Activate innate immunity to enhance humoral response. |
| Nod-like receptors (NLRs) | : are cytoplasmic sensors that detect microbial or nonmicrobial endogenous danger signals |
| inflammasome | multiprotein complex that induces cleavage of caspase-1 leading to secretion of IL-18 and IL 1beta. |
| IL-1β and IL18 activation: | beneficial role in promoting inflammation -secretion attracts immune cells to the site of infection. |
| Dysregulated inflammasomes - leading to subsequent overproduction of IL-1β and IL-18 can have detrimental effects, such as... | Autoimmune disorders, Crohn’s ,vitiligo, gout, asbestosis, Alzheimer’s disease - Non Immune related: metabolic syndrome, artherosclerosis |
| What are the two types of adaptive immunity? | Humoral and Cell Mediated Immunity |
| What are three types of T cells? | Regulatory, CD4 helper and CD8 cytolytic |
| What is humoral immunity good for? | extracellular invaders |
| What is cellular immunity good for? | intracellular microbes |
| Antibody Effector functions... | Complement activation Neutralization of toxins Opsonization and Phagocytosis Antibody-dependent cellular cytotoxicity (ADCC) |
| What is the only antibody that can pass the placental barrier and why is this important? | IgG, because rho antibodies can pass the placenta and kill the babies red blood cells. |
| The innate immune system... | provides second signals required for lymphocyte activation |
| What are the two requirements for adaptive immune response activation? | Signal 1 :Microbial antigen recognition provide signal 1 for the activation of the lymphocytes (recognize) Signal 2 : ensures immune responses are induced only when there is a dangerous infection (by inflammation) |
| What are second signals? | Second signals : act as co-stimulators a) For T cells: induced on host APCs by microbial products, during early innate response recognized by T cell receptors b) For B cells : products of complement activation recognized by B cell complement receptors |
| What is the clonal selection hypothesis? | Many clonal lymphocytes, each capable of recognizing a distinct antigenic determinant. When an antigen enters it activates a specific clone (1:100000); few lymphocytes will have the same receptor to that antigen. |
| Development and differentiation of different cell lineages... | depend on cell interactions with cytokines. |
| Lymphocytes that have CD 16 and CD 56 | natural killer cell; NK cells has some T cell makers but lack antigen specific receptors. NK cells have receptors to detect MHC class I (activating and Killer Inhibitory receptors,( KIR; Don't pass thru thymus. They also have Fc receptor for IgG. |
| NK T cells play a part in? | Asthma, and some cases of recurring pregnancy loss and preterm births in mice. |
| NK cells are... | tightly regulated by cytokines so that they don't induce autoimmunity |
| What markers tell us that it is a mature B cell? | CD 19, CD 21, FC receptors (to display their antibodies) and MHC class II receptors to display antigens |
| What is the most abundant lymphocyte in the blood and accessory lymph organs? | CD4 T helper lymphocyte |
| What happens to a monocyte normally? | it is a myeloid precursor to the macrophage. It circulates ~2 days in the blood and then enters tissue maturing to a macrophage. It can become activated and then specialize (ie kupffer cells) |
| B cells, macrophages and dendritic cells have what in common? | They are all Antigen presenting cell and therefore have MHC class II on their surface to present bacterial or viral material. |
| One function of IL-12 and what it is secreted by? | to recruit T-helper cell, and secreted by macrophage. |
| follicular dendritic cells are... | special non-phagocytotic antigen presenting cell. Express omplement receptors,Fc receptors and CD40 ligand; Not derived from precursors of bone marrow |
| follicular dendritic cells... | Function Display antigens on their surface to B cells to recognize antigens trapped by complement products and antibodies; Don't produce MHC class II receptors and therefore cannot present to T helper cells. Which makes sense b/c they are not a phagocyte |
| Neutrophils ( Main Role in Inflammation) | The most abundant circulating white blood cell –also called (PMN)- First cells to arrive at the site of Inflammation Multi-lobed nucleus, small pink granules Phagocytic, bactericidal, enzymatically digest microbes NOT APC; deficiency causes CG diseas |
| eosinophils | Bilobed nucleus, large pink crystal granules in cytoplasm Kill antibody coated parasites by exocytosis (e.g helminths) Heightened number in inflammatory infiltrates such as bronchial infections and asthma |
| Basophil | Bilobed nucleus, large blue granules, Non-phagocytic , In circulation , structural and functional similarities to mast cells Express high-affinity Fc receptors for IgE , Release active substances during allergic and hypersensitivity reactions |
| Mast Cell | Formed in the tissue from bone marrow precursor cells; Have granules with preformed mediators released after stimulation (histamine, prostaglandins and leukotrienes) Stimulation occurs by the anaphylotoxins or by cross-linking of surface IgE |
| Neutrophils in normal blood count? | 4400/ul Range 1800-7700/ul |
| Lymphocytes (B, T and NK) present in normal blood count? | 2500/ul 1000-4800/ul |
| eosinophils and basophils are raised in what type of response? | an allergic reaction (type I hypersensitivity) |
| In peripheral lymphoid organs (LN, Spleen lymphoid tissues)... | naive lymphocytes are activated by antigen to become effector cells to initiate induction of adaptive immunity |
| In generative lymphoid organs(Bone Marrow ,Thymus) | lymphocytes first express antigen receptors and attain maturity and clones develop |
| Naive T cells have | CCR7 receptor for recruitment in lymph node |
| Naive B cells | CXCR5 receptor for recruitment in lymph node |
| CD 3 | marker for T cells and specifically the two thymocytes: helper and cytotoxic |
| CD 4 | Class II MHC restricted T cells, thymocyte subsets, monocytes, macrophages. |
| CD 8 | class I MHC resrticted T cells |
| Your patient was found to have a spike of cells carrying the CD markers, 19, 20 and 40. What is the cell that was found to be high? | B cells carry all of these. |
| CD 16 A | macrophages and natural killer cells |
| CD 19 | B cells |
| CD 20 | B cells |
| CD 40 | B cells, macrophages, dendritic cells, and endothelial cells. |
| CD 45 | hematopoeitic cells |
| Natural killer cells have what as the cell surface markers? | CD 16 which binds the Fc region of IgG and MHC I cell surface receptors. |
| Cytokines? A) are soluble proteins produced in response to microbes B) regulate immunity C) Mediate communication amongst cells D) Are produced by leukocytes E) Are important in clinical medicine | All of these are correct answers and they act in an autocrine or paracrine manner |
| What can happen when the innate immune system releases too many cytokines? | septic shock; unlike the adaptive immune system, the innate immune system can release cytokines that produce systemic effects. The adaptive immune system only produces local effects. |
| What cytokine is involved in both innate and adaptive immunity? | Interferon gamma (guaranteed test question) |
| TNF | Produced by activated macrophages, T cells, mast cell IFN-γ augments TNF production by mast cells (TNF-α) T cells (TNF- β). |
| TNF at low concentration... | Stimulate recruitment of neutrophils and monocytes, stimulate vascular endothelial cells to express adhesion molecules and chemokines |
| TNF at moderate concentrations... | cause systemic effects( fever, cachexia by prostagladin synthesis in hypothalamus) |
| TNF at High concentrations | can lead to intravascular thrombosis and shock (clinical syndrome of septic shock) |
| Anti TNF drugs | Remicade (infliximab), Enbrel (etanercept) –bind to TNF receptor FDA approved for Rheumatoid Arthritis ,Crohn’s Disease, Ulcerative colitis |
| Fever is produced by TNF, but what other two cytokines are responsible? | IL 1 and IL 6 |
| IL-12... | is produced by macrophages and dendritic cells in early innate response. It recruits T helper, cytotoxic, and Natural killer cells (another innate immune cell), which causes them to increase their IFN-y production. It also enhances CD8 and NKs cytolytic a |
| IL-10 | Stops immune response! Produced mainly by activated macrophages and T regulatory cells Inhibits IL-12 production and expression co-stimulators and Class II MHC by activated macrophages and dendritic cells ( Anti-inflammatory cytokine) |
| IL-1 | Produced by activated macrophages ,endothelial cells , some epithelial cells , similar actions as TNF ( fever production and induces liver acute phase proteins) (pro-inflammatory cytokine ) |
| IL-6 | Produced by macrophages , endothelial cells, some T cells Promotes cell mediated immunity Induces proliferation of plasma B cells Stimulates pro-inflammatory cytokine IL-17 |
| IFN-α | produced by viral infected cells and mononuclear phagocytes; Increases expression class I MHC on infected cells and enhances killing by cytotoxic T Lymphocytes |
| IFN-B | produced by fibroblasts; the function is to inhibit viral replication; Increases expression class I MHC on infected cells and enhances killing by cytotoxic T Lymphocytes |
| Regulation of lymphocyte growth and differentiation? | IL-2, IL-4, IL-5, IFN –γ,TGF- β, IL-13, IL-17 produced mainly by T lymphocytes |
| TGF-β is produced by | T cells, macrophages and other cell types. |
| IL-2 | T cell growth factor (Naïve T cell , helper, cytotoxic , regulatory and memory T cell) |
| IL-4 | produced by Th2 cells and induce Inhibition of Th-1 cell development, B cell isotype switching to IgE, stimulates development of Th-2 cells from naïve CD4+ T cells Inhibition of Th-1 cell development |
| IL-5 | : produced by Th-2 and mast cells - activator of eosinophils to release granule contents in helminthic infections, B cell Ig switch to IgE |
| IL-13 | produced by Th-2 ,NK T & mast cells, Induces B cell Ig switch to IgE , increase epithelial mucus production |
| IFN-y | induces Th-1 and inhibits Th-2 cell production, Induces B cell isotype switch to opsonizing and complement- fixing IgG subclasses, Principal macrophage activating cytokine!(increases MHC I and MHC II on APCs ) |
| IL-17 | increase chemokine and cytokine production, activates neutrophils ,promotes inflammation |
| TGF-B | immunosuppressor for T cells and APCs , Induces B cell Ig switch to IgA, also induces tissue repair ,collagen synthesis |
| Hematopoeitic cytokines? | Stem cell factor, IL-3, IL-7, GM-CSF, G-CSF, M-CSF Produced by bone marrow stromal cells leukocytes and other cells. Stimulates growth and differentia- tion of bone marrow precursor cells |
| IL-7 | stimulates the lymphoid progenitor to differentiate into T and B cells. |
| TH1 subset of T helper are what? | Produce mainly IFN-γ, IL-2, TNF-α; involved in classical cell-mediated functions to combat viral infections & intracellular pathogens. Inflammation caused by Th1 and macrophages are the hallmarks of delayed type hypersensitivety (DTH ) reactions |
| TH2 subset of T helper... | Produce (IL-4, IL-5, IL-10, IL-13) – as a helper to B cell activation , respond to bacteria, helminthic parasites, and mediation of allergic reaction. Inhibit TH1. |
| TH 17 subset of T helper... | Produces IL-17 which is important for activation and recruitment of neutrophils. Highly proinflammatory/important mediators of tissue damage. |
| TH 17 are... | Naive CD4+ T Cells activated in the presence of TGFβ together with IL-6 or other inflammatory cytokines (IL-1β, and IL-23) become Th17 |
| What are the two most important immuno-suppressive cytokines? | TGF Beta, suppresses all T cells and APCs and IL-10, which suppresses TH1. |
| Chemokines | They are cytokines that stimulate chemotaxis of leukocytes from blood into tissues |
| Four families of chemokines : | (CC, C, CXC, CX3C)2 main classes: with promiscuous binding C-X-C receptors : CXCR1—CXCR8 C-C receptors : CR1-CCR11 majority of known chemokines are in these families Signal via : G-protein coupled receptors |
| CXCR4 | HIV coreceptor on T cells |
| CXCR5 | Receptor to recruit B cells to B cell zone of lymph node |
| CCR7 | T cell receptor to recruit to T cell zone of lymph node |
| CCR5 : | HIV coreceptor on Macrophage and DC |
| CXC chemokine IL-8 (produced by endothelial cells) binding to CXCR1 | recruits neutrophils The first responder |
| During homeostastis chemokines... | promote wound healing and angiogenesis |
| Idiotype | determined by heavy chain and light chain variable regions (antigen binding specificity) |
| PNP and ADA deficiency | causes Pro B or T not to mature to Pre B or T and therefore stops adaptive immunity causes SCID. |
| Omenn Syndrome | – lack immunoglobulin or TCRs because of lack of RAG |
| Deficiency C1 esterase inhibitor (C1 INH) | – Hereditary angioedema Type I (reduction in protein & function) type II (normal levels but decreased function) |
| Deficiency of DAF (Decay Activating Factor; CD55) | – Paroxysmal nocturnal hemoglobinuria (PNH) - Hemolysis Myeloproliferative disorder |
| DiGeorge Syndrome | Congenital aplasia or hypoplasia of the thymus Lymphopenia reflects decreased number of T cells Absent T cell function in peripheral blood Variable ab levels and function |
| Chronic Granulomatos Disease | Lack of Reactive Oxygen species in the macrophages |
| X-linked agammaglobulinemia (Bruton’s) | Recurrent pyogenic infections usually at 5-6 months Absence of B cells IgG <200 mg/dl with absence of IgA, IgM, IgD, IgE Very small tonsils Treat with gammaglobulin Found mostly in Males |
| Rheumatoid Arthritis | DRB1*0401,*0404 DRB1*0101 (DR4) |
| Type I Diabetes | DR3 and DR4 are the polymorphisms found in 25% |
| Multiple Sclerosis | DRB1*1501 DR 2 |
| Pemphigus vulgaris | DRB1*0402 (DR4) |
| Celiac Disease | DR3 DQ2(DQB1*0201, DQA1*0501) DQ8 |
| SLE | DR2/DR3 |
| Autoimmunity is caused by? | the environment, genetics, possibly drugs, hormones...it is a multifaceted phenomenon. |
| RA | Rheumatoid factor (85% of RA pts) which is antibody to the Fc portion of the host IgG. Generally of IgM class. May be seen in other diseases. This fixes complement and gets trapped in the joint in this case. |
| Autoimmunity is caused by? | the environment, genetics, possibly drugs, hormones...it is a multifaceted phenomenon. |
| RA | Rheumatoid factor (85% of RA pts) which is antibody to the Fc portion of the host IgG. Generally of IgM class. May be seen in other diseases. This fixes complement and gets trapped in the joint in this case. |
| Hashimoto’s thyroiditis | Lymphocytic infiltration by CD8 T cells and B cells which may form lymphoid follicles with plasma cells Autoantibodies which stimulate the growth and division of thyroid cells Circulating lymphocytes which are sensitized to thyroid antigens |
| Type I Diabetes | Anti-islet cell antibodies (ICA);Reported that many patients develop anti-ICA months or even years before clinical symptoms Anti-ICA will diminish in frequency to 5-10% in patients with long-standing type I DM Class II HLA antigens DR3 and/or DR4 |
| pernicious anemia | Parietal cell antibody is found in 85-90% of patients and inhibits the secretion of intrinsic factor |
| Primary Biliary Cirrhosis | Progressive inflammatory destruction and obliteration of intrahepatic bile ducts, followed by development of cirrhosis and liver failure Major Immunologic Features Over 99% of patients have detectable antimitochondrial antibodies |
| Celiac Disease | Characterized by villous atrophy and malabsorption. Hypersensitivity to various cereal grain storage protein and most commonly those found is wheat gluten and more precisely a substance derived from gluten know as gliadin. DQ2, DQ8 and DR3 polymorphisms |
| Goodpasture's Syndrome | Anti-basement membrane antibodies binding to antigens of the glomerular and alveolar basement membranes Antibodies are type II or cytotoxic type Complement is activated by the Ag-Ab reactions Linear deposition of IgG and complement on glomerular baseme |
| Linear Reactions are... | type II hypersensitivity |
| Granular looking... | type III hypersensitivity immune complexes. |
| Rhematic Fever | Caused by group A streptococcal infection. Antibodies to that look like things on cardiac muscle. |
| C 22 | Is the core peptide of Hepatitis C virus. |
| HCV antibody results can be misleading so | MUST GIVE INDEXES with response Significant index depends on method Bayer Chemiluminesence (>11.0) Abbott EIA (>3.8) Ortho Chemiluminesence (>8.0) |
| Acute Infection with Hepatitis B leads to what being detected by serology? | Hepatitis B surface antigen (HBsAg) IgM anti-Hepatitis B core (HBcIgM) |
| Chronic Infection with hepatitis B, then this will be detected in patients serum. | Hepatitis B surface antigen (HBsAg); persistence in the serum |
| If patient is immune to Hep B, what will be detected in their titer? | HBsAb |
| Chronic Lymphocytic Leukemia | B Cells expressing CD19, CD20 and CD5 Treatments may be a humanized monoclonal antibody to CD20 (Rituximab) or CD52 (Campath-1H) |
| Type I or immediate type hypersensitivity | a.) Sensitization b.) Production of IgE c.) Sensitization of Mast cells/basophils by IgE d.) Cross-linking of IgE by re-exposure to allergen |
| What mast cells release | (1.) Histamine (Spasmogen) (2.) Neutrophil Chemotactic Factor (3.) Eosinophilic Chemotactic Factor of Anaphylaxis (ECF-A) (4.) Tryptase (Activates C3) (5.) Kininogenase It also makes: Leukotrienes, prostoglandins, and thromboxane from AA. |
| IL-3 | Mast Cell proliferation factor |
| TNF-a | promotes inflammation, recruitment of other leukocytes |
| Generally what do the things released from Mast Cells do? | Cause vasodialation, vascular permeability, bronchoconstriction, mucus secretion, chemotaxis, and an increase in TH2 CD4 cells. |
| RAST | Class 0 <0.35 IU/ml Absent Class 1 0.36-0.7 IU/ml Low Class 2 0.71-3.5 IU/ml Moderate Class 3 3.51-17.5 IU/ml High Class 4 17.51-50.0 IU/mlVery High Class 5 50.1-100 IU/ml Very High Class 6 >100 IU/ml Very High Titers to IgE antibody |
| Blood transfusion reaction is? | is a type II reaction. This is a reaction against RBCs, WBCs, and platlets via IgM and IgG (not IgE like the type I response). |
| Good Pastures, Myastenia Gravis and Graves disease | Are type II reactions Good Pasture's Disease is to the glomular basement membrane |
| What is C2a? | Product of complement that is a Prokinen (causes edema). It is inhibited by C1 -INH. |
| What is C3a? | It is a product of complement that causes anaphylatoxin (mast cell degranulation, enhanced vascular permeability, anaphylaxis. |
| What is C3b? | It is a product of complement that is an opsonin. It can activate phagocytosis by binding to complement binding sites on macrophages. It is inhibited by factor H and Factor I. |
| C4a | Product of complement: anaphylatoxin, but less potent |
| C4b | opsonin (phagocyte activation) Inhibited by C4-BP & Factor H |
| C5a | (chemotactic factor)-anaphylactic as C3a-much more potent(attracts PMN and activates basophil, mast cells) Inhibited by C3a-INA. |
| C5b67- | For chemotaxis, Inflammation, attaches to other membranes It is inhibited by Protein S |
| C1 inhibitor is used to shut down the serine proteases of the classical complement pathway. If a patient is deficient in C1-inhibitor what will occur? | hereditary angioedema. They will not be able to stop producing complement anaphylatoxins. |
| What happens to a patient with hereditary C3 deficiency? | They will get chronic pyogenic infections, due to decrease in the complement systems abilities. |
| What does DAF do? | It inhibits C3 convertase. Therefore inhibiting opsonin and anaphylatoxin being made. Shuts down complement. It is found on epithelial cells. |
| C4 binding protein does what? | Shuts down the classical complement pathway. |
| C1 INH | dissociates C1r and C1s from active C1 complex, therefore inhibiting the classical complement pathway. |
| Factor H and Factor I together | cleave C3b, therefore inhibiting its opsonizing effects. It becomes iC3b. iC3b has many other signaling functions including stimulation of phagocytosis. |
| The smaller cleavage products C3a, C4a, C5a, called "anaphylatoxins" can do what? | Apart from attracting phagocytes, they cause mast cell degranulation and enhance vessel permeability facilitating access of plasma proteins and leukocytes to the site of infection |
| What does the complement system promote? | Inflammation, through its anaphylatoxin products, opsonization and phagocytosis through C3b and iC3b respectivly, and most importantly lysis through the membrane attack complex. |
| A deficiency of these components of the classical complement pathway C1,C2,C4 would cause what? | Predisposition to SLE with increased precipitation of Immune complexes in tissues and Inflammation |
| Deficiency of the MBL complement pathway causes what? | Suceptibility to bacterial infections in infants. Have inability to initiate lectin pathway |
| Deficiency of Factors B or D can cause? | Suceptibility to pus forming bacterial infections - lack of sufficient opsonization of bacteria |
| Deficiency of DAF and CD59 can cause? | Causes paroxysmal nocturnal hemoglobinuria - inherited deficiency |
| C9 and MAC formation deficiency? | Lack of terminal components C5-C9 causes repeated Neisseria infections and impaired bactericidal activity. |
| Anergy: | a state of unresponsiveness to subsequent activation stimuli (a mechanism of peripheral tolerance to self antigens or non-dangerous antigens. Because to get a complete activation we need TCR binding and a second signal. |
| Regulatory T cells | Express FoxP3 and CD 25. There is tremendous potential for controlling autoimmune diseases by regulating these cells. |
| IL-1 | activates B cells, T cells, and hematopoietic differentiation. |
| IL-6 | both a pro-inflammatory and anti-inflammatory cytokine. |
| Etanercept (Enbrel): | fusion protein that binds TNF receptors and blocks TNFa and TNFb binding, RA treatment |
| Infliximab (Remicade): | anti-TNFa antibody that blocks TNFa binding, RA treatment |
| Kineret: | recombinant IL-1Ra; blocks IL-1 binding, RA treatment |
| Natalizumab (Tysabri): | humanized monoclonal antibody against VLA-4 (integrin-a4) which is present on leukocytes and mediates binding to VCAM-1 on inflamed endothelium and other receptors necessary for leukocyte migration. – used in treatment of MS and Chrohn’s |
| H1 receptors | are found in the smooth muscle of the intestines, bronchi, and blood vessels. |
| H2 receptors are in | airway mucous, gastric parietal cells and in the vascular and central nervous Example: Cimetidine targets H2 receptors |
| autoimmune disease | has to involve a T cell recognizing an auto-antigen. There may be many reasons why the immune system suddenly has no anergy to self. Ultimately CD4 cells drive the damage. |
| SLE | DR2/3 |
| RA | DR4 |
| MS | DR2 |
| Systemic Lupus Erythmatosis | Generalized disorder that expresses itself predominately as a system vasculitis of unknown cause Most commonly found in young females (15-35 years) Anti-dsDNA (50-75%) and anti-Smith (Sm; 20-30%) antibodies Criteria(4 or more of 11 criteria) |
| Rheumatoid Factor | is frequently an IgM antibody against the hosts IgG Fc region. It is found in 85% of people with RA but is not a must to have RA. |
| In Hashimotos Thyroiditis | Virtually 100% of patient’s will be reactive to thyroglobulin and/or thyroid microsomal antigen (specific antigen in microsomal fraction is Thyroid Peroxidase) |
| Diabetes | Insulin autoantibodies (IAA) are found in a large majority of newly diagnosed patients Anti-islet cell antibodies (ICA); 90% of newly diagnosed cases |
| Over 99% of patients have detectable antimitochondrial antibodies | Primary Biliary Cirrhosis |
| Antinuclear Antibodies | Detection and identification can be helpful in the differential diagnosis of patients with autoimmune or connective tissue disorders. However, the presence must ALWAYS be considered with the PATIENTS HISTORY. |
| We will have a low titer ANA even in normal people. Nuclear antibodies are sometimes present for infection, pregnancy, etc True or False | True |
| HLA B27 | 90% likely hood of having Ankylosing Spondylitis |
| 1:160 for a good | titer |
| homogeneous ANA is found for | dsDNA, histones and chromatin. Found in SLE. |
| Speckled ANA patterns | Anti Smith or Anti RNP or SSa and SSb |
| Centromere ANA | CREST syndrome |
| Anti-lamins | Detected as Lamin A/C and Lamin B Detected in diverse conditions but primarily in SLE and liver disease |
| ribosomyl-P cytoplasmic pattern | SLE patients with severe depression or psychosis (45-90%) |
| Anti-mitochondria cytoplasmic pattern | Diseases Primary Biliary Cirrhosis (95%) Scleroderma (3-10%) Antigens Detected on the inner mitochondrial membrane Cloned and available in ELISA format |
| In Celiac disease | Transglutaminase is a repair enzyme which deaminates gliadin & adds glutamate to an existing peptide. High concentrations in connective tissue. The immune system recognizes tTG in combination with gliadin as a neoantigen. |
| TYPE IV HYPERSENSITIVITY DELAYED TYPE HYPERSENSITIVITY | Tuberculin-Type Hypersensitivity Granulomatous Hypersensitivity Contact Hypersensitivity Jones-Mote Cutaneous Basophil Hypersensitivity Delayed Type Hypersensitivity - Cell Mediated Immunity Your T cells will attack you! |
| Hapten small inorganic molecule that will bind to a protein | and produce Type 4 hypersensitivity reaction. It causes T cells to attack your own cells because of the inorganic molecule. |
| Contact dermatitis | is type 4 |
| immediate reactions, for example to peanuts are | type I hypersensitivity reactions. These reactions are caused by IgE mediated mast cell responses. |
| Cytotoxic or type II reactions | are mediated by antibodies to the cell of choice. Mostly in blood transfusions. |
| Graft vs host disease | is caused when the bone marrow of a host is destroyed to have a bone marrow transplant. The graft then attacks the host. results in death. |
| IFN a and b | stop viral replication |
| bDNA chiron test | Branched DNA testing or bDNA testing is a test created by the Chiron company to measure the viral load of HIV in a sample of blood. |
| Positive single stranded ribonucleic acid (+ ssRNA) flavivirus Virions per day of one trillion Diversity/complexity Six significant genotypes | Hep C virus |
| Acute Infection 15-25% will resolve HCV infection 75-85% will become chronically infected by HCV Chronic infection (75-85% of those infected with HCV) 80% will remain stable progresses to | 10-20% will progress to cirrhosis Cirrhosis (10-20% of Chronically Infected) 75% will slowly progress 25% will progress to hepatocelluar carcinoma Hepatocellular Carcinoma, Transplant, Death (25% of Cirrhosis) |
| Serology Molecular Assays (NAT, PCR, bDNA, TMA, etc) | used to test for antibodies used to test for viral load |
| Possibilities of weak positive | False positive Patient in seroconversion Resolved infection and titer on decline Immunosuppressed HIV Transplant Chemotherapy |
| Chronic Lymphocytic Leukemia (CLL) | B Cells expressing CD19, CD20 and CD5 Treatments may be a humanized monoclonal antibody to CD20 (Rituximab) or CD52 (Campath-1H) |
| Tetany is a medical sign, the involuntary contraction of muscles, caused by diseases and other conditions that increase the action potential frequency. | Usually seen with Di George syndrome. The absence of thymus and parathyroid gland. |
| Extracellular bacteria | Gram Positive Cocci Staphylococcus, Streptococcus, Enterococcus, etc Gram Positive Rods Corynebacterium, Gardnerella vaginalis, etc Gram Negative Bacteria Escherichia, Shigella, Salmonella |
| What do Extracellular bacteria do? | .) Secrete repellents or toxins that inhibit chemotaxis, secrete IL-10 or secrete soluble receptors 2.)Capsules or outer coats which inhibit attachment by the phagocyte 3.) Release factors that block triggering of killing mechanisms 4.)Secrete catala |
| Mycobacteria | intracellular bacteria |
| TH2 dominant– allergic reactions – drives antibody responses – good at fighting parasites and other extracellular invaders. | shuts down macrophages with IL-10 |
| Intracellular bacteria | Several organisms (e.g. Mycobacterium) can escape from the phagosome to multiply in the cytoplasm 9.) The organism (e.g. M. tuberculosis) may kill the phagocyte |
| Immunity to Fungi is principally Cellular Involving: | Lymphocytes, NK cells, Macrophages Fungi are not normally susceptible to direct killing by antibody and complement. Patients with neutropenia or defective neutrophil function appear predisposed to disseminated infection with yeastlike fungi (e.g. Candid |
| killing of parasites | is TH2 mediated and antibody dependent. |
| Antibody Dependent Cellular Toxicity | What is required for parasitic clearance. |
| Natural Active Immunity and induced active immunity | Got infected naturally, developed response; vaccination |
| Side Effects of Vaccines | Reversion to virulence Encephalitis (swelling of brain) Allergic reactions due to egg protein, antibiotics, preservatives, etc Undesired “passenger” viruses Local reaction Type 3 reaction (you already have abs to it) |
| To get better responses to vaccines | You can conjugate the epitope from the microbe to a protein so that it is internalized by your neutrophils and a true B and T cell response is mounted. |
| Induced Passive Immunity | Gammaglobulin for antibody to infectious agents, Erythroblastosis fetalis (RhoGAM), anti-venom |
| main reason for vaccines | to eradicate disease |
| recurrent fungal infections suggests what? | T cell deficiency because fungus cannot easily be destroyed by humoral responses or complement. |
| Recurrent infections with Staph suggests what? | That they have a problem mounting extracellular responses. B cells either don't work or are absent. |
| Microcidal ability (NBT, Chemiluminesence, Neutrophil Oxidative Index (NOI), Killing curve) | Tell you whether or not your phagocytes work. |
| Test complement by? | Quantitation 1.) Total complement (CH50) 2.) Individual complement components (e.g. C2, C4, C3, etc) b. Function 1.) Total complement (CH50) |
| Pyogenic bacteria is primarily extracellular whereas viral and fungal infections are primarily intracellular. True or False | True |
| RAG and PNP/ADA deficiencies cause? | Autosomal SCID |
| Btk deficiency? | X-linked agammaglobinemia. This is a deficiency in B cells with a normal number of working T cells. |
| gamma c deficiency? | X-linked SCID. This is a deficiency in T cells with a normal number of functioning B cells. |
| X-linked hyper IgM | due to a lack of the CD 40 ligand preventing the B cell from interacting with the T cell and producing other Igs. |
| Lack of Class II MHC on B cells cause bare lymphocyte syndrome which is... | caused by mutation in genes encoding transcription factors required for class II MHC gene expression. This means that B cells will not be able to present foreign antigens to T cells and will therefore not be able to produce T cell dependent responses. |
| Defects in T cell receptor complex expression or signaling cascade | Cause Decreased t cell or abnormal ratios of CD4 to CD8. Decreased cell mediated immunity. Rare cases due to mutation or deletions of CD3 proteins ZAP-70. |
| X-linked agammaglobulinemia (Bruton’s) | Recurrent pyogenic infections (extracellular infection) usually at 5-6 months. Absence of B cells IgG <200 mg/dl with absence of IgA, IgM, IgD, IgE Very small tonsils Treat with gammaglobulin Males |
| Common variable immunodeficiency disease | Recurrent pyogenic infections with onset at any age Total immunoglobulins : <300 mg/dl with IgG <250 mg/dl B cells usually normal in number High incidence of autoimmune disease Affects both males and females |
| Selective IgA deficiency | IgA <5 mg/dl with other Igs being normal or increased Cell mediated immunity is Increased association with allergies, recurrent sinopulmonary infections Increased autoimmune disease Incidence is 1:600 to 1:80; most common of immunodeficiency |
| Hyper IgM syndrome | Increased levels of IgM (150 – 1000 mg/dl Generally inherited in an X-linked manner; also acquired X-linked form is associated with genetic defect in the CD40 ligand (CD154); no isotype switch. Again pyogenic infections because limited extracell respo |
| Chronic Mucocutaneous Candidiasis | Selective T cell defect in responding to Candida B cells intact with normal ab response |
| Absent T cells and normal or increased number of nonfunctioning B cells (T-, B+) | X-Linked SCID 40-50% of SCID cases Mutation in the gene encoding of the gamma chain of the IL-2 receptor, located on the X chromosome |
| Autosomal Recessive SCID | Identical phenotype of the X-linked SCID group and cannot be distinguished clinically Mutation in the JAK3 tyrosine kinase (responsible for transmitting signals) |
| If IL-2 can't bind to the T cell then. | The patient will have an inability to mount T cell responses. IL-2 is an important T cell growth factor. |
| Presence of normal numbers of T cells & B cells (T+, B+)is caused by: | Bare lymphocyte syndrome Lack expression of HMC class I, w/ or w/o class I expression. Circulating T & B cell numbers may be normal; however, in the absence of MHCII no foreign ag presented. Mutation is in the gene encoding the activator for the HLA. |
| Wiskott-Aldrich | Immunodeficiency with thrombocytopenia, eczema Diagnosed by presence of WAS gene X-linked Hypercatabolism of Ig Serum IgM usually low with elevated serum IgA and IgE B cells are normal in number but patient fails to form ab following immunization sug |
| Ataxia-Telangiectasis | Clinical onset by 2 years of age Autosomal recessive; AT locus mapped to 11q23 Usually immunodeficiency of IgA, IgE and IgG2 with a moderate reduction in T cell counts and responses. sinus in common Involves neurologic, vascular, endocrine and immune |
| LAD 2 | Mutations in gene encoding a protein required for synthesis of the sialyl-Lewis X component of E and P selectin Ligands |
| Complement C2 and C4 deficiency | Mutations in C2 and C4 genes. Deficient activation of classical pathway and failure to fight of immune complexes and also pyogenic, or other extracellular infections. |
| Chronic granulomatous Disease | recurrent infections with catalase-positive bacteria and fungi X-linked (most common) and autosomal recessive Four major forms of CGD X-linked – deficiency of cytochrome b588 (CGD X91) Autosomal recessive – deficiency in NADPH oxidase (CGD A47) |
| Diagnosis by nitrobluetetrazolium test (NBT), neutrophil oxidative index (NOI), quantitative killing curve | Chronic Granulomatous Disease People with this have recurrent osteomyelitis. |
| Cediak Higashi | is a deficiency of phagocytes. Causes decreased NK cell activity and abnormal PMN chemotaxis. Abnormal lysosomal enzyme level. Increased infections. partial albinism. |
| LAD 1 and LAD II are what? | A beta integrin and selectin defect that causes abnormal inflammatory response, no pus, recurrent extracellular bacterial infections. Impaired wound healing. delayed umbilical separation. cell count 2-20 times normal in absence of infection. |
| Hyper IgE, Defective Chemotaxis, Eczema & Recurrent Infection | IgE concentrations in excess of 5000 IU/ml Eosinophilia Diminished ab response following immunization |
| DAF (Decay Activating Factor; CD55) – | Deficiency causes Paroxysmal nocturnal hemoglobinuria (PNH) - Hemolysis, Myeloproliferative disorder |
| Secondary acquired immunodeficiency can be caused by | infection, malignant neoplastic diseases, autoimmune diseases, immunosuppressive treatments, or surgery. |
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