Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Immunology
FA complete review
| Question | Answer |
|---|---|
| What are the two primary organs of the immune system? | Bone marrow and Thymus |
| What happens in the bone marrow? | Immune cell production and B-cell maturation |
| T cell maturation occurs in the ________. | Thymus |
| What is the role of the secondary organs of the immune system? | Allow immune cells to interact with antigen |
| Which are the secondary immune system organs? | Spleen, lymph nodes, tonsils, and Peyer Patches |
| What is a lymph node? | Secondary lymphoid organ that has many afferents and 1 or more efferents. |
| What is the function of a lymph node? | 1. Nonspecific filtration by macrophages, 2. Storage of B and T cells, and 3. Immune response activation |
| Which part of the lymph node contains B cells? | Follicle |
| How are primary follicles? | Dense and dormant |
| Which kind of follicles have pale central germinal centers and are active? | Secondary follicles |
| Which follicle are active? | Secondary |
| What immune cells are located in the follicles of a lymph node? | B-cells |
| What are the medullary cords? | Closely packed lymphocytes and plasma cells |
| What is the lymph node medulla composed of? | Medullary cords and medullary sinuses |
| Medullary cords + Medullary sinuses = | Lymph node medulla |
| What is the role of medullary sinues? | Communicate with efferent lymphatics and contain reticular cells and macrophages |
| What cells are contained in the medullary sinuses? | Reticular cells and macrophages |
| What is a reticular cell? | A fibroblast that synthesizes collagen alpha-1(III) |
| Which part of the lymph node houses T cells? | Paracortex |
| Which cells are found in the Paracortex of the lymph ndode? | T cells |
| Where is the Paracortex located? | Region between the follicles and medulla |
| Which part of lymph node is not well developed in patients with DiGeorge syndrome? | Paracortex |
| What is inside the Paracortex? | High in endothelial venules through which T and B cells enter from blood |
| An extreme cellular immune response, causes an enlargement of which region of the lymph node? | Paracortex |
| Head and neck drain lymph into which lymph node? | Cervical |
| What are the associated pathologies of defective Cervical lymph node drainage? | - URT infection - Infectious mononucleosis - Kawasaki disease |
| EBV-mononucleosis will show _____________ lymph node enlargement. | Cervical |
| What areas of the body drain their lymph into the Mediastinal cluster? | Trachea and Esophagus |
| Primary lung cancer may cause a defective _________________ lymph node cluster drainage. | Mediastinal |
| Lung's lymph node cluster is: | Hilar lymph node cluster |
| Which areas drain lymph into the Axillary lymph node? | Upper limbs, breast, sine above umbilicus |
| Associated pathologies of the Axillary lymph node cluster. | Mastitis and Metastasis |
| Celiac lymph node cluster receives drainage from: | Liver, stomach, spleen, adn upper doudenum |
| The Upper duodenum lymph is drained into the _____lymph node cluster. | Celiac |
| What areas drain lymph into the Superior Mesenteric lymph node? | Lower duodenum, jejunum, ileum, colon to splenic flexure |
| Where does lymph form the lower duodenum drains? | Superior Mesenteric lymph node cluster |
| Lymph produced by the section of the colon to the splenic flexure drains into the ____________________ lymph node cluster. | Superior Mesenteric |
| Area of body drained: Colon from splenic flexure to Upper rectum. | Inferior Mesenteric |
| What are the most common pathologies associated with abnormal lymph drainage of the Celiac, Superior, and Inferior lymph node clusters? | 1. Mesenteric lymphadenitis 2. Typhoid fever 3. Ulcerative colitis 4. Celiac disease |
| Ulcerative colitis may have defective lymph drainage of which lymph node clusters? | Celiac, Superior, and Inferior Mesenteric lymp nodes |
| The Para-aortic lymph nodes drain with body areas? | Testes, ovaries, kidneys, and uterus |
| Where do teste lymph fluid drain into? | Par-aortic lymph node cluster |
| Ovaries and Uterus drain lymph into the _____________ cluster. | Para-aortic |
| STDs are associated pathologies of defective _____________ and ____________ lymph node clurester drainage. | Internal Iliac and Superficial inguinal |
| The internal iliac lymph node cluster receives drained lymph fluid from: | Lower rectum to anal canal (above pectinate line), bladder, vagina (middle third), cervix and prostate. |
| BPH is associated with ineffective lymph drainage the by the ______ lymph node cluster. | Internal iliac |
| WHich lymph node cluster drains below the pectinate line? | Superficial inguinal |
| Skin below the umbilicus, except for popliteal area, is drained by the _______________________________ lymph node cluster. | Superficial inguinal |
| Scrum and vulva lymph fluid drain into the _______. | Superior inguinal lymph node |
| What is drained by the Popliteal Node cluster? | Dorsolateral foot and posterior calf |
| Foot/leg cellulites is associated with: | Infective Popliteal lymph drainage |
| Which are the non-palpable lymph nodes? | Mediastinal, Hilar, Celiac, Para-aortic, and Internal Iliac |
| What is drained by the Right Lymphatic duct? | Right side of body above diaphragm into junction of the right subclavian and internal jugular vein |
| Which lymph node cluster are included or drain into the Right Lymphatic duct? | Right sided Cervical, Mediastinal, Hilar, and Axillary |
| Where is the Spleen anatomically located? | LUQ of abdomen, anterior to left kidney, protected by 9th - 11th ribs |
| Which ribs protect the spleen? | 9th to 11th left sided ribs |
| What are Sinusoids of the spleen? | Long, vascular channels in the red pulp with fenestrated "barrel hoop" basemente membrane |
| What is in the White Pulp of the spleen? | Follicle (B cells) and Periarteriolar lymphoid sheath (T cells) |
| PALS stands for: | Periarteriolar lymphatic sheath |
| Where is PALS locaed? | Within the White Pulp |
| Where in the Spleen are T cells found? | In the PALS |
| What cells are in the Follicle of the White pulp of the spleen? | B cels |
| What is the mane of the area between the Red and White pulp in the Spleen? | Marginal zone |
| What cells are located in the Marginal zone of the Spleen? | Macrophages and specialized B cells |
| What happens in the Marginal Zone of the Spleen? | Antigen-presenting cells (APCs) capture blood-borne antigens for recognition by lymphocytes. |
| What is the role of Splenic macrophages? | Remove encapsulated bacteria |
| What are the results of Splenic dysfunction? | Decreased IgM --> decrease complement activation ---> decreased C3b opsonization --> leading to increased susceptibility to encapsulated organisms. |
| Functional asplenic patients have increased susceptibility to __________ organisms. | Encapsulated |
| What are Post-splenectomy blood findings? | 1. Howell-Jolly bodies 2. Target cells 3. Thrombocytosis 4. Lymphocytosis |
| Where is the Thymus located? | Anterior Superior mediastinum |
| What is the site of T-cell differentiation and maturation? | Thymus |
| How is the Thymus in DiGeorge syndrome and SCID? | Hypoplastic |
| The thymus is derived from the ________ pharyngeal pouch. | Third |
| What is contained in the Medulla of the Thymus? | Mature T cells and Hassall corpuscles containing epithelial reticular cells |
| CXR of normal neonatal thymus shape? | "sail-shaped" |
| Neoplasm of thymus | Thymoma |
| What are conditions associated with Thymoma? | Myasthenia gravis and Superior vena cava syndrome |
| What are the main two types of immunity? | Innate and Adaptive immunity |
| What are the components of Innate immunity? | Neutrophils, macrophages, monocytes, dendritic cells, NK cells, complement, physical epithelial barriers, and secreted enzymes |
| How is resistance of Innate immunity? | Resistance persists generations; does not change within an organism's lifetime |
| How is response to pathogens in the Innate immunology? | -Nonspecific -Occurs rapidly - NO memory response |
| Which type of immunity has No memory response to pathogens? | Innate immunity |
| What secreted proteins in the Innate immunity? | Lysozyme, complement, C-reactive protein (CRP), defensins |
| TLR are key features of ______________ immune system. | Innate |
| What are Toll-like receptors? | Pattern recognition receptors that recognize pathogen-associated molecular patterns (PAMPs) and lead to activation of NF-kB |
| TLRs recognize _____________ to activate ______________. | TLRs -----> PAMPS ---> NF-kB |
| What are some common PAMPs? | 1. LPS (gram (-) bacteria 2. Flagellin (bacteria) 3. Nucleic acids (viruses) |
| What is the common PAMP found in viruses? | Nucleic acids |
| LPS is: | PAMP found in gram negative bacteria |
| What are the components of Adaptive immune system? | T cells, B cells, and circulating antibodies |
| The variation through V(D)J recombination during lymphocyte development. It describes? | Mechanism of action of the Adaptive immunity |
| How is the response to pathogens in Adaptive immunity? | Highly specific, refined over time. Develops over long periods; Memory |
| Memory repose is faster and more robust. Seen in what type of immunity? | Adaptive |
| What are the secreted proteins of Adaptive immunity? | Immunoglobulins |
| What is the key feature of Adaptive immunity? | Memory cells |
| What are memory cells featured in the Adaptive immune system? | Activated B and T cells; subsequent exposure to a previously encountered antigen ---> stronger, quicker immune response |
| What encodes the MHC? | HLA genes |
| What is the function of the MHC? | Present antigen fragments to T cells and bind T-cell receptors (TCRs) |
| What are the loci of MHC I? | HLA-A, HLA-B, and HLA-C |
| MHC I present antigens to T cells and bind to which kind of receptors? | TCR and CD8 |
| 1 long chain, 1 short chain. Describes the structure of what kind of MHC? | MHC I |
| Which type of cells express MHC I? | All nucleated cells, APCs, platelets |
| Which cells do not express MHC I? | RBCs |
| What is the function of MHC I? | Present ENDOGENOUSLY synthesized antigens to CD8+ cytotoxic T cells |
| Organelle in which MHC I antigen peptides are loaded on? | Rough Endoplasmic Reticulum |
| What is the delivery method used by MHC I ? | TAP (transporter associated with antigen processing) |
| What is the associated protein in MHC I? | B2-microglobulin |
| Loci in MHC II? | HLA-DP, HLA-DQ, and HLA-DR |
| Binding receptors of MHC II? | TCR and CD4 |
| Which MHC is composed by 2 equal-length chains? | MHC II |
| What are the chains the make up the structure of the MHC II? | 2 alpha and 2 beta chains |
| Which cells are the only ones that express MHC II? | APCs |
| What is the function of MHC II? | Present EXOGENOUSLY synthesized antiges to CD4+ helper T cells |
| MHC I act on _________________________ T cells. | CD8 + cytotoxic |
| MHC II act on ________________________ T cells. | CD4+ helper |
| Describe antigen loading in MHC II? | Antigen loaded following release of invariant chain in an acidified endosome |
| Which MHC class is associated with an Invariant chain? | MHC II |
| What condition is associated with HLA A3? | Hemochromatosis |
| Associated diseases of HLA B8? | Addison disease, myasthenia gravis, Graves disease |
| HLA B27 associated diseases: | 1. Psoriatic arthritis 2. Ankylosing spondylitis 3. IBD-associated arthritis 4. Reactive arthritis |
| Celiac disease is associated with HLA __________. | DQ2/DQ8 |
| Which conditions are associated with HLA DR2? | Multiple sclerosis, hay fever, SLE, and Goodpasture syndrome |
| Which HLA subtype is associated with Multiple sclerosis? | DR2 |
| SLE is associated with which HLA subtypes? | DR2 and DR3, |
| What are the conditions often seen with HLA DR3 association? | DIabetes mellitus type I, SLE, Graves disease, Hashimoto's thyroiditis, and Addison disease |
| The mnemonic 2-3, SLE is used for: | Indicate that SLE has HLA DR2 and HLA DR3 associations |
| Rheumatoid arthritis is associated with HLA _____. | DR4 |
| DM type I has which HLA subtype associations? | DR3 and DR4 |
| Which condition has a HLA DR5 association? | Hashimoto thyroiditis |
| Which condition has HLA B8, HLA DR3, and HLA DR4 associations? | Addison disease |
| What does HLA stand for? | Human Leukocyte antigens |
| What is the use of HLA proteins in the immune system? | Aid to recognize which cells belong to our body and which do not. |
| Which is a common lymphocyte member of the innate immune system? | Natural killer cells |
| What enzymes are used by NK cells? | Perforin and granzymes |
| What is the purpose of NK cell to use perforin and granzymes? | Induce apoptosis of virally infected cells and tumor cells |
| Which cytokines enhance the activity of Natural killer ells? | IL-2, IL-12, IFN-alpha, and IFN-B |
| When are NK cells induced to "kill"? | 1. As they are exposed to nonspecific activation signal on target cell and/or, 2. to an absence of MHC I on target cell surface. |
| What is a second way NK cells kill? | Via antibody-dependent cell-mediated cytotoxicity |
| CD16 binds to Fc region of bound Ig. Describes? | NK cell kill method via antibody-dependent cell-mediated cytotoxicity |
| CD16 is associated with ____________ cells. | Natura killer |
| What are the 4 major functions of B cells? | 1. Humoral immunity 2. Recognize antigen 3. Produce antibody 4. Maintain immunologic memory |
| How do B cells recognize antigens? | Undergo somatic hypermutation to optimize antigen specificity |
| How are B cell able to produce antibodies? | Differentiate into plasma cells to secrete specific immunoglobulins |
| What kind of cell does a B cell needs to differentiate into, in order to produce antibodies? | Plasma cell |
| What are the main functions of T cells? | 1. Cell-mediated immunity 2. CD4+ cells help B cells make antibodies and produce cytokines 3. CD8+ T cells directly kill virus-infected cells 4. Delayed cell-mediated hypersensitivity (Type IV) 5. Acute and chronic cellular organ rejection |
| What is the purpose of CD4+ T cell interaction with B cells? | Create antibodies and produce cytokines to recruit phagocytes and activate other leukocytes |
| What kind of T cell is found in the Cortex of the thymus? | CD4+CD8+ T cell |
| Positive selection of T cells occurs in the ______________________. | Cortex of the thymus |
| The Thymic medulla is the site of: | 1. Negative selection 2. Production of CD8+ T Cells and CD4+ T cells |
| What are the 4 most common derivatives of a Helper T cell? | Th1, Th2, Th17, and Treg |
| Helper T cell + IL-12 and IFN-gamma ===> | Th1 |
| Th2 are produced by interaction of: | Helper T cell and IL-2 + IL-4 |
| IL-4 and IL-10 can inhibit the production of: | Th1 cells |
| What cytokine is used to create Treg cells? | TGF-beta |
| TGF-B + IL-6 working on a Helper T cell produce what T cell subtype? | Th17 |
| Where are T cell precursors found? | Bone marrow |
| Positive selection: | T cells expressing TCRs capable of binding self-MHC on cortical epithelial cells survive. |
| Negative selection: | T cells expressing TCRs with high affinity for self antigens undergo apoptosis or become regulatory T cells |
| Immunodeficiency due to Th1 cell dysfunction | Mendelian susceptibility to mycobacterial disease |
| What is the function of Th1 cells? | Activates macrophages and cytotoxic T cells to kill phagocytosed microbes |
| What cytokine is primarily secreted by Th1 cells? | IFN-gamma |
| What is the function Th2 cells? | Activate eosinophils and promote production of IgE for parasite defense |
| Cytokines secreted by Th2 cells: | IL-4, IL-5, IL-6, IL-10, and IL-13. |
| Which Th1 cytokine inhibits Th2 cell secretions? | IFN-gamma |
| Th17 cell function: | Immunity against extracellular microbes, through induction of neutrophilic inflammation |
| What cytokines are secreted by Th17 cells? | IL-17, IL-21, IL-22 |
| What immunodeficiency is related to Th17 cells dysfunction? | Hyper-IgE syndrome |
| What it the role or function of Treg cells? | Prevent autoimmunity by maintaining tolerance to self-antigens |
| IL-6 inihitos the function of ________________cells. | Treg |
| IPEX is due to _____________________ immunodeficiency. | Treg cell |
| What does IPEX stand for? | Immunodysregulation Polyendocrinopathy Enteropathy X-linked |
| Rare disease linked to dysfunction of the transcription factor FOXP3, widely considered the master regulator of regulatory T cell linage (Treg). Dx? | IPEX syndrome |
| Cytokines secreted by Treg cells? | TGF-B, IL-10, and IL-35 |
| What are interleukins? | Group of cytokines expressed on white blood cells |
| How is the macrophage-lymphocyte interaction enhanced? | By interaction of T cell CD40L with CD40 on macrophages. |
| Which cytokine works to enhance the function of macrophages to kill microbes? | IFN-gamma |
| What cells are killed by cytotoxic T cells? | Virus-infected, neoplastic, and donor graft cells by inducing apoptosis. |
| Regulatory T cells work by: | Help maintain specific immune tolerance by suppressing CD4 and CD8 T-cell effector functions. |
| Which markers are seen on Treg cells? | CD3, CD4, CD25, and FOXP3. |
| What are the clinical features of IPEX syndrome? | Enteropathy, endocrinopathy, nail dystrophy, dermatitis, and/or other autoimmune dermatologic conditions |
| What is an important associated of IPEX syndrome? | Diabetes in male infants |
| What are the APCs? | B cells, dendritic cells, Langerhans cells, and macrophages |
| What is the "Signal 1" in T cell activation? | Antigen is presented on MHC II and recognized by TCR on Th (CD4+) cell |
| What is the "Signal 2" in T cell activation? | Costimulatory signal via interaction of B7 protein (CD80/86) on dendritic cell and CD28 on naive T cell |
| What is the B7 protein marker on Dendritic cells? | CD80/86 |
| Activated B cell can undergoes: | Class switching, affinity maturation, and antibody production |
| What ligand-receptor on B cell activation is required to reach class switching? | CD40 receptor on B cell binds CD40 ligand on Th cell |
| What is the "Fab" region in antibody structure made of? | Light (L) and heavy (H) chains recognized antigens |
| Which part of the antibody is in charge of antigen recognition? | Fab segment |
| What region on the antibody structure fixes complement? | Fc region of IgM and IgG |
| Heavy chain in antibody structure contributes to ____ and_____ regions. | Fc and Fab |
| The light chain of an antibody only contributes to which region? | Fab |
| What does the Fab determine? | Idiotype; unique antigen-binding pocket; only 1 antigenic specificity expressed per B cell |
| What are characteristics of Fc region? | Constant, Carboxy terminal, Complement binding, Carbohydrate side chains |
| Which region of an antibody determines isotype? | Fc region |
| Which are common isotypes determined by Fc? | IgM, IgD, etc |
| Example of generation of antibody diversity | Random recombination of VJ (Light-chain) or V(D)J (heavy chain) genes |
| The addition of random nucleotides to DNA during recombination by terminal TdT, is an example of? | Generation of antibody diversity |
| Somatic hypermutation and affinity maturation, represents a form of: | Generation of antibody specificity |
| The generation of antibody diversity is antigen _____________. | Independent |
| Generation of antibody diversity occurs: | Independently from antigen |
| Generation of Antibody specificity is --> | Antigen dependent |
| What is the type of generation of antibody specific seen in the constant region? | Isotype switching |
| Somatic hypermutation and affinity maturation causes generatio on specificity in the _____________. | Variable region |
| Opsonization is: | Antibody promotes phagocytosis |
| Antibody prevents bacterial adherence | Neutralization |
| What is the definition of Complement activation? | Antibody activates complement, enhancing opsonization and lysis. |
| Complement binding occurs ithe __________ of the Fc region. | CH-2 |
| The CH-3 part of the Fc region, allows for ___________ binding. | Macrophage |
| Macrophage binding can occur in the ____________ and ____________ of the Fc region. | CH2 and CH3 |
| VH + CH1 = | Fab region |
| Where are the variable regions in the structure on an antibody? | In the distal tips of the Fab region |
| Main antibody in secondary response to antigen. | IgG |
| What is the most abundant immunoglobulin isotype in the serum? | IgG |
| What are the roles of IgG? | 1. Fixes complement 2. Opsonized bacteria 3. Neutralizes bacterial toxins and viruses |
| Which is the only Ig isotype that can cross the placenta? | IgG |
| Which immunoglobulin isotype provides infants with passive immunity? | IgG |
| Why can IgG provide passive immunity to infants? | It can cross the placenta |
| How is IgA found when it is barely secreted? | Dimer form |
| How is the dimer formed by secreted IgA connected? | By a J chain |
| IgA --> | Prevents attachment of bacteria and virues to mucus membranes |
| Which immunoglobulin prevents the attachment of bacteria or viruses to mucous membranes? | IgA |
| IgA does ______________________. | Not Fixes complement |
| What GI structure produces IgA? | Peyer patches |
| What is a common infection protected by IgA? | Giardia |
| Which the most produced Ig isotype? | IgA |
| Serum concentrations of IgA are _______. | Low |
| IgA is secreted into: | Saliva, tears, mucus and breast milk |
| What is an important feature of IgA associated with epithelial cells? | Picks up secretory component form epithelial cells, which protects the Fc protion from luminal proteases |
| Produced in the primary (immediate) response to an antigen. | IgM |
| Fixes complement, Cannot cross placenta, Antigen receptor on the surface of B cells | IgM |
| What form is IgM when secreted? | Pentamer |
| What is the advantage of Pentamer IgM? | Enables avid binding to antigen while humoral response evolves |
| Which immunoglobulin may be found in a pentamer? | IgM |
| Which immunoglobulin still has an unclear function? | IgD |
| To which cells does IgE bind to? | Mast cells and Basophils |
| What are functions of IgE? | 1. Cross-links when exposed to allergen 2. Immediate (type 1) hypersensitivity through release of inflammatory mediators such as histamine |
| How does IgE is involved in parasite immunity? | By activating eosinophils |
| Which immunoglobulin is found with the LOWEST serum concentration? | IgE |
| Classification of antigen lacking a peptide component. | Thymus-independent |
| Which are the Thymus-dependent antigens? | Antigens containing a protein component |
| What is key of vaccines made from Thymus-independent antigens? | Require booster and adjuncts |
| Diphtheria vaccine is made from what kind of antigens? | Thymus-dependent antigens |
| What is the complement system? | System of hepatically synthesized plasma proteins that play a role in innate immunity and inflammation. |
| What are the activation pathways of Complement? | Classic, Alternative, and Lectin |
| Which immunoglobulins mediate the Classic Complement pathway? | IgG and IgM |
| What activates the Alternative complement pathway? | Microbe surface proteins |
| Mannose is used as sugar that activates which complement pathway? | Lectin |
| What are the 2 primary opsonis in bacterial defence? | C3b and IgG |
| What process is enhanced by Opsonins? | Phagocytosis |
| What is a secondary function of C3b? | Clear immune complexes |
| Main function of C3b? | Opsonization |
| Which complement components are involved mainly in Anaphylaxis? | C3a, C4a, and C5a |
| C5a is involved in which two complement roles? | 1. Anaphylaxis 2. Neutrophil chemotaxis |
| What is the function of C5b-9? | Cytolysis by MAC |
| What is the main role of complement inhibitors? | Prevent complement activation on self cells |
| What are the two main types of complement inhibitors? | Decay-accelerating factor (DAF) and C1 esterase inhibitor |
| What is another form to refer to Decay-accelerating factor (DAF)? | CD55 |
| What are complications of Early complement protein deficiency? | Increased risk of severe, recurrent pyogenic sinus and respiratory tract infections, and increased risk of SLE. |
| Increased susceptibility to recurrent Neisseria bacteremia is seen with what kind of complete deficiencies? | Terminal complement deficiencies (C5-C9) |
| What are the "early" complement components? | C1 - C4 |
| What are the two main Complement regulatory protein deficiencies? | 1. C1 esterase inhibitor deficiency 2. Paroxysmal nocturnal hemoglobinuria |
| What is caused in C1 esterase inhibitor deficiency? | Hereditary angioedema due to unregulated activation of kallikrein leading to elevated levels of bradykinin |
| How is the level of serum C4 in C1 esterase inhibitor deficiency? | Low |
| ACE inhibitors are contraindicated in which Complement disorder? | C1 esterase inhibitor deficiency |
| What is the MCC of Paroxysmal nocturnal hemoglobinuria? | Defect in PIGA gene preventing the formation of anchors for complement activation |
| Which anchors are commonly prevented to form in Paroxysmal Nocturnal hemoglobinuria (PNH)? | Decay-accelerating factor (DAF/CD55) and membrane inhibitor of reactive lysis (MIRL/CD59) |
| What important cytokines are exclusively secreted by macrophages? | IL-1, IL-6, IL-8, IL-12, and TNF-alpha |
| What are the actions performed by IL-1? | Fever, acute inflammation, and activates the osteoclast-activating factor |
| What chemokine is activated by IL-1? | Osteoclast-activating factor |
| IL-6 produces: | Fever and stimulates production of acute-phase proteins |
| Acute-phase proteins are produced by _______. | IL-6 |
| Major chemotactic factor for neutrophils | Interleukin-8 |
| What is functions of IL-12? | - Induces differentiation of T cells into Th1 cells - Activates NK cells |
| The formation of Th1 cells is due to the action of which macrophage secreted cytokine? | IL-12 |
| Secondary action of IL-12? | Activation of NK cells |
| What macrophage-secreted cytokine activates the endothelium? | Tumor necrosis factor - alpha |
| What are some actions caused by TNF-a? | WBC recruitment and vascular leak |
| What is the role of TNF-a in malignancy? | Causes cachexia |
| What is cachexia? | Weakness and wasting of the body due to severe chronic illness |
| Which macrophage-secreted cytokines mediate fever and sepsis? | IL-1, IL-6, and TNF-alpha |
| What is a shared role of IL-1, IL-6, and TNF-alpha? | Mediation of fever and sepsis |
| Which two important cytokines are secreted by all T cells? | IL-2 and IL-3 |
| IL-2 stimulates __________________. | T cells |
| IL-3 stimulates _________________ _________________. | Bone marrow |
| IL- 1: _______________ (_____) | Fever (hot) |
| IL-4: stimulates ____________________ production | IgE |
| What interleukin stimulates the IgE production? | IL-4 |
| IL-5: stimulates __________ production | IgA |
| Which important cytokine stimulates the production of IgA? | IL-5 |
| IL-6: stimulates ________________________________ production | Acute-phase protein |
| What are the roles and actions of IL-2? | Stimulates growth of helper, cytotoxic, and regulatory T cells, an NK cells |
| Which cytokine helps the growth many T cells and NK cells? | IL-2 |
| Which interleukin stimulates the growth and differentiation of bone marrow stem cells? | IL-3 |
| IL-3 works similarly to _______________. | GM-CSF |
| What is GM-CSF? | Substance that helps make more white blood cells, especially granulocytes, macrophages, and cells that become platelets |
| What is the cytokine secreted by Th1 cells? | Interferon - gamma |
| When is IFN-gamma secreted? | Secreted by NK cells and T cells in response to antigen or IL-12 form macrophages |
| What is the role of IFN-gamma on macrophages? | Stimulate macrophages to kill phagocytose pathogens |
| What cell differentiation is inhibited by Interferon gamma? | Th2 |
| What are two secondary actions of IFN-gamma? | 1. Activated NK cells to kill virus-infected cells 2. Increases MHC expression and antigen presentation by all cells |
| What are the 3 main cytokines produced exclusively by Th2 cells? | IL-4, IL-5, and IL-10 |
| What interleukin is involved in the differentiation of T cells into Th2 cells? | IL-4 |
| What type of class switching is promoted by IL-4? | Class switching to IgE and IgG |
| Promotes growth of B cells | IL-4 |
| What cytokine promotes the class switching to IgA? | IL-5 |
| Stimulates growth and differentiation of eosinophils | IL-5 |
| Which Th2 cytokine is known to attenuate the inflammatory response? | IL-10 |
| Besides Th2 cells, what other T cell subtype secretes IL-10? | Treg cells |
| What are some actions of IL-10? | 1. Decreases expression of MHC II and Th1 cytokines 2. Inhibits activated macrophages and dendritic cells |
| Which two well known cytokines attenuate the immune response? | TGF-Beta and IL-10 |
| What is the respiratory burst? | Rapid release of reactive oxygen species (ROS), superoxide anion, and hydrogen peroxide, from different cell types. |
| Another way to refer to the Respiratory burst is as _____________ _____________. | Oxidative burst |
| What needs to be activated in order for the respiratory burst to initiate? | Phagocyte NADPH oxidase complex |
| What is Myeloperoxidase? | Contains a blue-green heme-containing pigment that gives sputes its color |
| What enzyme gives sputum is characteristic color? | Myeloperoxidase |
| What is the role of NADPH in the respiratory burst? | Once is activated it plays role in both the creation and neutralization of ROS |
| Why are CGD patients at increased risk of infection by catalase positive species? | These species are capable of neutralizing their won H2O2, leaving phagocytes without ROS for fighting infections |
| What P. aeruginosa product helps kill pathogens? | Pyocyanin |
| What is Lactoferrin? | Protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation |
| What neutrophil protein helps immune system fight infection via iron chelation? | Lactoferrin |
| How does the Oxidative burst helps the release of lysosomal enzymes? | It leads to K+ influx, which releases lysosomal enzymes from proteoglycans |
| What metal is required by Gluthatione peroxidase (involved in oxidative burst) to work? | Selenium |
| Interferons alpha and beta are part of which type of viruses innate host defense? | RNA and DNA viruses |
| What are interferons? | Glycoproteins synthesized by virus-infected cells that act on local cell, "priming them" for viral defense by downregulating protein synthesis to resist potential viral replication and upregulate MHC expression to facilitate recognition of infected cells |
| Interferons are said to: | Interfere with viruses |
| CD3 is associated with: | TCR for signal transduction |
| WHat T cell surface marker signals transduction? | CD3 |
| What are the most relevant T cell makers? | TCR, CD3, and CD28 |
| A CD28 positive T cell binds _________________. | B7 on APC |
| Cell surface marker proteins of helper T cells? | CD4, CD40L, and CXCR4/CCR5 |
| Co-receptor for HIV | CXCR4/CCR5 |
| CD8 | Cell surface marker protein of cytotoxic T cells |
| CD4 and _______________ are the Treg cell surface marker proteins. | CD25 |
| Which B cell surface marker binds to antigen? | Ig |
| What CDs are classically expressed in B cell surface? | CD19, CD20, CD21, and CD40 |
| Which cell surface marker on B cells is receptor for EBV? | CD21 |
| MHC II and B7 are both cell surface markers seen in which cell? | B cells and Macrophages |
| Which macrophage cell surface protein serves as receptor for PAMPs? | CD14 |
| What type of cell is positive for CD14, CD40, and CCR5? | Macrophage |
| What B7 marker is found in macrophages? | CD80/86 |
| Which macrophage surface protein serve as receptors for enhancing phagocytosis? | Fc and C3b |
| What CDs are found on NK cells? | CD16 and CD56 |
| CD56 is suggestive marker for _______ cells. | NK |
| What is the cell surface marker of Hematopoietic stem cells? | CD34 |
| What is anergy? | State during which a cell cannot become activated by exposure to its antigen |
| When are T and B cells anergic? | When exposed to their antigen without costimulatory signal (signal 2). |
| Anergy is considered other mechanism of ________________. | Self-tolerance |
| Missing which signal in T cell activation leads to a state of anergy? | Signal 2 |
| How is passive immunity acquired? | Receiving preformed antibodies |
| Which type of immunity is seen with a rapid onset? | Passive |
| Short duration of immune response is seen with _________________ immunity. | Passive |
| What are common examples of Passive immunity? | 1. IgA in breast milk 2. maternal IgG crossing placenta 3. Antitoxin 4. Humanized monoclonal antibody |
| What is the means of acquisition of Active immunity? | Exposure to foreign antigens |
| How is the duration and onset of Active immunity? | Slow onset but long-lasting duration |
| Which type of immunity has memory, Passive or Active? | Active |
| Slow onset and long lasting protection are key features of _____________ immunity. | Active |
| What are common examples depicting Active immunity? | Natural infection, vaccines, an toxoid |
| Which infection are often treated with combined passive and active immunizations? | Hepatitis B and Rabies |
| A vaccination induces: | Active immune response (humoral and/or cellular) to specific pathogens |
| What are the 4 MC types of vaccines? | 1. Live attenuated vaccine 2. Killed or inactivated vaccine 3. Subunit 4. Toxoid |
| Description of a live attenuated vaccine | Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host. Induces cellular and humoral response. |
| What kind of active immune response is induced by Live attenuated vaccine? | Humoral and cellular immunity. |
| What vaccine is alright to be applied to HIV patients with CD4 count greater than 200 cells/mm3? | MMR and varicella vaccines |
| What are some cons of Live Attenuated vaccine? | May revert to virulent form. Often contraindicaed in preganancy and immunodeficeincdy. |
| List of Live attenuated vaccine: | 1. Adenovirius 2. Sabin Polio 3. Varicella (chickenpox) 4. Smallpox 5. BCG 6. Yellow fever 7. Influenza (intranasal) 8. MMR 9. Rotavirus |
| Which type of influenza vaccine is live attenuated? | Intranasal |
| Sabin polio vaccine is an ______________________- vaccine | LIve attenuated |
| Pathogen is inactivated by heat or chemicals. Maintaining epitope structure on surface antigens is important for immune response. | Killed or inactivsted vaccine |
| Which type of vaccine only induces humoral resonse? | KIlled or inactivated vaccine |
| Which are safer vaccines, Live or kiIled? | Killed |
| Weaker immune response; booster shots usually required. | Killed or inactivated vaccine |
| Examples of Killed or Inactivated vaccine: | Rabies, Influenza (injection), Polio (Salk), hepatitis A |
| What type of Polio vaccine is killed vaccine? | Salk |
| What is an subunit vaccine? | Includes only the antigens that best stimulate the immune system |
| What are some common subunit vaccines? | HBV, HPV, acellular pertussis, Neisseria meningitis, Streptococcus pneumoniae, Haemophilus influenza type b |
| What are Toxoid vaccines? | Denatured bacterial toxin with an intact receptor binding site. |
| What are some examples of Toxoid vaccines? | Clostridium tetani and Corynebacterium diphtheriae |
| What is the hypersensitivity type I? | Anaphylactic and atopic |
| What is the Immediate phase of Type I hypersensitivity? | Antigen cross links preformed IgE on pre sensitized mast cells leading to release of histamine and tryptase |
| What is marker for mast cell activation? | Tryptase |
| What substances are released in the early phase of Type I hypersensitivity reaction? | Histamine and Tryptase |
| What cells are involved in the late type I hypersensitivity reaction? | Chemokines and cytokines |
| What lab technique is used to identify the allergen specific for IgE in Type I hypersensitivity reactions? | ELISA |
| Which hypersensitivity reaction is Antibody-mediated? | Type II |
| What are the 3 main results seen in Type II hypersensitivity? | Cellular destruction, inflammation, and cellular dysfunction |
| What happens in Cellular destruction in Type II hypersensitivity? | Cell is opsonized (coated) by antibodies, leading to: - Phagocytosis and/or activation of complement system - NK cell killing (antibody-dependent cellular cytotoxicity) |
| What are examples of Type II hypersensitivity due to cellular destruction? | 1. Autoimmune hemolytic anemia, 2. Immune thrombocytopenia 3. Transfusion reactions 4. Hemolytic disease of the newborn |
| What conditions are Type II hypersensitivity and due to antibodies binding to cell-surface antigens causing inflammation? | - Goodpasture syndrome - Rheumatic fever - Hyperacute transplant reaction |
| Cellular dysfunction due to a Type II hypersensitivity causes which conditions? | Myasthenia gravis, Graves disease, and Pemphigus vulgaris |
| How is inflammation causes in type II hypersensitivity reaction? | Activation of complement system and Fc receptor-mediated inflammation |
| Abnormal blockade or activation of downstream process after antibodies bind to cell surface receptors. Dx? | Cellular dysfunction in a type II hypersensitivity reaction |
| What is the pathogenesis of Type III hypersensitivity? | Immune complex-antigen-antibody complexes activate complement, which attracts neutrophils, which then release lysosomal enzymes. |
| Serum sickness is a type ______ hypersensitivity | 3 |
| What type of hypersensitivity is Arthurs reaction? | Type 3 |
| What is Serum Sickness? | Antibodies to foreign proteins are produced and 1-2 weeks later, antibody-antigen complexes form and deposit in tissues leading to complement activation and eventually inflammation and tissue damage |
| Reaction of foreign proteins. | Serum sickness |
| What is Arthurs reaction? | Intradermal injection of antigen into a presensitized individual leads to immune complex formation in the skin. |
| What are the clinical manifestations of Arthurs reaction? | Edema, necrosis and activation of complement after intradermal injection of an antigen. |
| What are common examples of Type 3 hypersensitivity reaction associated with vasculitis and systemic manifestations? | 1. SLE 2. Polyarteritis nodosa 3. Poststreptococcal glomerulonephritis |
| What drugs are associated with Serum sickness-like reactions? | Drugs that act as haptens (penicillins) and infection such as HBV |
| What are the clinical manifestations of Serum Sickness-like reactions? | Fever, urticaria, arthralgia, proteinuria, and lymphadenopathy occur 1-2 weeks after antigen exposure. |
| What cells are involved in Type IV hypersensitivity? | T cells |
| What are two mechanisms of actions seen in Type 4 hypersensitivity? | 1. Direct cell cytotoxicity: CD8+ cytotoxic T cells kill targeted cells 2. Inflammatory reaction: effector CD4+ T cells recognize antigen and release inflammation-inducing cytokines |
| Which hypersensitivity type does not involve antibodies? | Type IV |
| What are common examples of Type IV hypersensitivity conditions? | Contact dermatitis, Graft-vs-Host disease |
| What are common tests based off the Type IV hypersensitivity? | PPD (tuberculosis infection) Patch test (cause of contact dermatitis) Candida extract (T cell immune function) |
| Pathogenesis of Allergic/Anaphylactic reaction to blood transfusion. | Type I hypersensitivity reaction against plasma proteins in transfused blood. |
| IgA deficient individual must receive what kind of blood procuts? | IgA-free produces to avoid an anaphylactic blood transfusion reaction |
| What are key features of Allergic/anaphylactic reaction to a blood transfusion? | Quick (minutes to 3 hours); Urticaria, fever, hypotension, respiratory arrest and shock |
| What is the timing on Febrile nonhemolytic transfusion reaction? | Within 1-6 hours |
| What are the two known mechanisms of Febrile nonhemolytic transfusion reaction? | 1. type II Hypersensitivity reaction with host antibodies against donor HLA and WBCs 2. Induced by cytokines that are created and accumulate during storage of blood produces |
| What is the pathogenesis of Acute hemolytic transfusion ratin? | Type II hypersensitivity reaction. Intravascular or extravascular hemolysis. |
| What causes Intravascular hemolysis in Acute hemolytic transfusion reaction? | ABO blood group incompatibility |
| Host antibody reaction against foreign antienge on donor RBCs, causes what kind of hemolysis in Acute hemolytic transfusion reaction? | Extravascular |
| What is the clinical presentation of Acute hemolytic transfusion reaction? | Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria, and jaunce. |
| What is the pathogenesis of Transfusion-related acute lung injury? | Donor anti-leukocyte antibodies against recipient neutrophils and pulmonary endothelial cells |
| Respiratory distress and noncardiogenic pulmonary edema are often part of the clinical presentation of what type of Blood transfusion reaction? | Transfusion-related acute lung injury |
| Which are the exclusive B cell immunodeficiencies? | 1. X-linked (Bruton) agammaglobulinemia 2. Selective IgA deficiency 3. Common variable immunodeficiency |
| Which are the exclusive T cell immunodeficiencies? | 1. Thymic aplasia (DiGeorge syndrome) 2. IL-12 receptor deficiency 3. Autosomal dominant Hyper-IgE syndrome (Job syndrome) 4. Chronic mucocutaneous candidiasis |
| What is the main defect of Bruton agammaglobulinemia? | Defect in BTK, a tyrosine kinase gene --> no B-cell maturation. |
| What is the clinical presentation of Bruton agammaglobulinemia? | Recurrent bacterial and enteroviral infections after 6 months |
| What gender is vastly more affected in Bruton agammaglobulinemia? | Young boys |
| What is the inheritance mode of Bruton agammaglobulinemia? | X-linked recessive |
| What are the key findings of Bruton agammaglobulinemia? | Absent B cells in peripheral blood, decreased Ig of all classes. Absent lymph nodes and tonsils. No live vaccines |
| What isotypes of immunoglobulins are low n Bruton agammaglobulinemia? | All Ig classes |
| What is the most common Primary immunodeficiency? | Selective IgA deficiency |
| Anaphylaxis to IgA-containing products. Low IgA and normal IgG and IgM levels. | Selective IgA deficiency |
| What kind of infection is at increased risk in Selective IgA deficiency? | Giardiasis |
| Defect in in B cell differentiation. Suspected immunodeficiency? | Common variable immunodeficiency |
| What age is commonly seen CVID? | After 2 years of age |
| What are some key features and characteristics of CVID? | 1. Risk of autoimmune disease 2. Bronchiectasis 3. Lymphoma 4. Sinopulmonary infections |
| What are the classical findings in CVID? | Decreased plasma cells and immunoglobulins |
| Common name for Thymic aplasia | DiGeorge syndrome |
| What gene deletion is seen DiGeorge syndrome? | 22q11 |
| What pharyngeal pouches are underdeveloped in DiGeorge syndrome? | 3rd and 4th Pharyngeal pouches |
| What is the result of underdeveloped pharyngeal pouches in DiGeorge syndrome? | Absent thymus and parathyroids |
| What are some important features of DiGeorge syndrome? | 1. Tetany due to hypocalcemia 2. Recurrent viral/fungal infections due to T cell deficiency 3. Conotruncal abnormalities |
| What are the common conotruncal abnormalities seen in DiGeorge syndrome? | Tetralogy of Fallot and Truncus arteriosus |
| What is a key finding on CXR of a patient with DiGeorge syndrome? | Absent thymic shadow |
| Absent thymic shadow on CXR + Low T cells, hypocalcemia, and decreased PTH. Dx? | DiGeorge syndrome |
| Calcium serum level in DiGeorge syndrome? | Hypocalcemia |
| Inheritance mode of IL-12 receptor deficiency | Autosomal recessive |
| What immunodeficiency is due to a decreased Th1 response? | IL-12 receptor deficiency |
| What is the clinical presentation of IL-21 receptor deficiency? | Disseminated mycobacterial and fungal infections; may present after administration of BCG vaccine |
| What immunodeficiency is often seen develop after administration of BCG vaccine? | IL-12 deficiency |
| What is the key clinical finding of IL-12 receptor deficiency? | Decreased interferon (IFN)- gamma |
| Common name for Autosomal dominant hyper-IgE syndrome? | Job syndrome |
| What is the pathogenesis of Job syndrome? | Deficiency in Th17 cell due to STAT3 mutation --> impaired recruitment of neutrophils to sites of infection |
| What are key findings of Job syndrome? | Increased IgE and Eosinophils |
| What common mnemonic is used to describe the clinical features of Job syndrome? | FATED |
| The mnemonic "FATED" in Job syndrome stands for: | F- coarse Facies A - cold staphylococcal Abscesses T- retained primary Teeth E- increased IgE D - Dermatologic problems (eczema) Bone fracture at minor trauma |
| Person with multiple rows of teeth. Dx? | Job syndrome |
| Which immunodeficiency is associated with cold (noninflamed) staphylococcal abscesses? | Job syndrome |
| Congenital defects in IL-17 or IL-17 receptors. Dx? | Chronic mucocutaneous candidiasis |
| Noninvasive Candida albicans infections of skin and mucous membranes. Dx? | Chronic mucocutaneous candidiasis |
| No reaction to Candida antigens. Dx? | Chronic mucocutaneous candidiasis |
| Which immunodeficiencies involve B and T cells? | Severe combined immunodeficiency (SCID), Ataxia-telangiectasia, Hyper-IgM syndrome, and Wiskott-Aldrich syndrome (WAS) |
| What are the 2 main defects leading to SCID? | 1. Defective IL-2R gamma chain (X-recessive) 2. Adenosine deaminase deficiency (Autosomal recessive) |
| What is the common clinical picture of SCID? | Failure to thrive, chronic diarrhea, thrush. Recurrent viral, bacteria, fungal, and protozoal infections. |
| Findings of SCID? | Decreased T-cell receptor excision circles (TRECs). Absence of thymic shadow (CXR), germinal centers, and T cells |
| Defective in ATM gene. Dx? | Ataxia-Telangiectasia |
| What is the triad seen in Ataxia-Telangiectasia? | 1. Cerebellar defects (Ataxia) 2. Spider Angiomas (telangiectasia) 3. IgA deficiency |
| What malignanices are increased risk in Ataxia-Telangiectasia? | Lymphoma and leukemia |
| What serum marker is increased in Ataxia-Telangiectasia? | AFP |
| Decreased levels of IgA, IgG, and IgE. Lymphopenia and cerebellar atrophy. Finding commonly seen in: | Ataxia-Telangiectasia |
| What is the MCC of Hyper-IgM syndrome? | Defective CD40L on Th cells --> class switching defect |
| Which immunodeficiency is due to defective class switching? | Hyper-IgM syndrome |
| Mode of inheritance of Hyper-IgM syndrome? | X-linked recessive |
| What are common opportunistic infections in Hyper-IgM syndrome? | Pneumocystis, Cryptosporidium, and CMV |
| Severe pyogenic infections in early life. Immunodeficiency? | Hyper-IgM syndrome |
| Which immunoglobulins are decreased in Hyper-IgM syndrome? | IgG, IgA, and IgE |
| The failure to make germinal centers and normal to slightly elevated IgM. Immunodeficiency? | Hyper-IgM syndrome |
| Mutation in WASp gene. Dx? | Wiskott-Aldrich syndrome |
| What is the result of the WASp gene? | Leukocytes and platelets unable to reorganize actin cytoskeletal --> defective cytoskeleton |
| Clinical finding found in Wiskott-Aldrich syndrome are summarized using what mnemonic? | WATER: W- Wiskott-Aldrich syndorme T- Thrombocytopenia E- Eczema R- Recurrent (pyogenic) infectious |
| Which immunoglobulins are elevated in WAS? | IgE and IgA |
| Which immunodeficiency is seen with fewer and smaller platerls? | Wiskott-Aldrich syndrome |
| What are the 3 immunodeficiency due to phagocyte dysfunction? | 1. Leukocyte adhesion deficiency (type 1) 2. Chediak-Higashi syndrome 3. Chronic granulomatous disease |
| What is the main defect in development of Leukocyte adhesion deficiency type I? | LFA-1 integrin (CD18) protein on phagocytes |
| Defective LFA-1 integrin protein. Dx? | Leukocyte adhesion deficiency (type 1) |
| Defective LFA-1 integrin protein causes? | Impaired migration and chemotaxis due to phagocyte dysfunction |
| Absent pus lesions. Key of which immunodeficiency? | Leukocyte adhesion deficiency (type 1) |
| What are the most common clinical features of LAD type 1? | - Recurrent skin and mucosal bacterial infections - Absent pus - Impaired wound healing - Delayed (>30 days) separation of umbilical cord |
| What key findings in LAD type 1? | Increased neutrophils in blood, but absence of neutrophils at infection sites. |
| Neutrophilia but no neutrophils at infected sites. Dx? | Leukocytes adhesion deficiency (type 1) |
| What are the deficits leading to Chediak-Higashi syndrome? | 1. Defect in lysosomal trafficking regulator gene (LYST) 2. Microtubule dysfunction in phagosome-lysososme fusion |
| What are findings in Chediak-Higashi syndrome? | Giant granules in granulocytes and platelets. Pancytopenia Mild coagulation defects |
| What are the main Chediak-Higashi syndrome clinical features? | Progressive neurodegeneration Lymphohistiocytosis Albinism (partial) Recurrent pyogenic infections by staphylococci and streptococci Peripheral Neuropathy |
| Recurrent pyogenic infection by Staph and Strep. Dx? | Chediak-Higashi syndrome |
| What enzyme is defective in Chronic Granulomatous disease? | NADPH oxidase |
| What is the result of deficentive NADPH oxidase? | Decreased reactive oxygen species and decreased respiratory burst in neutrophils |
| Increased susceptibility to catalase (+) organism. Dx? | Chronic granulomatous disease |
| Negative Nitroblue tetrazolium dye reduction test. Dx? | Chronic granulomatous disease |
| What test are abnormal and /or negative in CGD? | 1. Dihydrorhodamine test 2. Nitroblue tetrazolium dye reduction test |
| B-cells deficiencies tend to produce recurrent _________________ infections. | Bacterial |
| T-cell deficiencies produce more ________ and ___________ infections. | Fungal ; Viral |
| Graft from self | Autograft |
| Graft from nonidentical individual of the same species | Allograft |
| What kind of graft is form different species? | Xenograft |
| Pathogenesis of Hyperacute transplant rejection. | Pre-existing recipient antibodies react to donor antigen, activate complement. |
| Features of Hyperacute transplant rejection. | Widespread thrombosis of graft vessels --> ischemia/necrosis |
| Which transplant rejection has an onset of weeks to months? | Acute transplant rejection |
| What is the cellular pathogenesis seen in Acute transplant rejection? | CD8+ T cells and/ or CD4+ T cells activated against donor MHCs |
| What is the main difference in pathogenesis in hyperacute and humoral acute transplant rejection? | Acute transplant rejection develops antibodies after transplant |
| Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate. Features of what kind of transplant rejection. | Acute transplant rejection |
| Hyperacute, acute, and chronic transplant are examples of __________________ disease. | Host-vs-Graft |
| What is the pathogenesis of Chronic transplant rejection? | CD4+ T cells respond to recipient APCs presenteing donor peptides, including allogeneic MHC. |
| What is the general clinical features of Chronic transplant rejection? | Recipient T cells react and secrete cytokines --> proliferation of vascular smooth muscle, parenchymal atrophy, and interstitial fibrosi. Dominated by arteriosclerosis. |
| What is the example of lung chronic transplant rejection? | Bronchiolitis obliteran |
| What is accelerated atherosclerosis? | Heart manifestation of chronic transplant rejection |
| What is the pathogenesis of GVHD? | Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with "foreign" proteins --> organ dysfunction . |
| GVHD is a Type ____ hypersensitivity reaction. | IV |
| Which organs or tissues are the most affected with GVHD? | Bone marrow and Liver |
| Why are liver and bone marrow most affected with GVHD? | Rich in lymphocytes |
| What are actions and purposes of immunosuppressants? | Block lymphocyte activation and proliferation |
| What are two common Calcineurin inhibitors? | Cyclosporine and Tacrolimus |
| Cyclosporine inhibits Calcineurin by binding to _______________. | Cyclophilin |
| Which action is produced by Cyclosporine, Tacrolimus, and Sirolimus? | Blocks T-cell activation |
| What is the most important adverse effect of Cyclosporine? | Nephrotoxicity |
| What are some effects of cyclosporine toxicity? | Nephrotoxicity, hypertension, hyperlipidemia, neurotoxicity, gingival hyperplasia, and hirsutism |
| Tacrolimus inhibits calcineurin by inhibiting __________ protein. | FK506 |
| Which interleukin response is inhibited which immunosuppressants? | IL-2 |
| What is the mechanism of action of Sirolimus? | mTOR inhibitor; binds FKBP |
| What is another name for Sirolimus? | Rapamycin |
| What are the toxicity signs of Sirolimus? | Pancytopenia, insulin resistance, hyperlipidemia |
| Which calcineurin inhibitor is NOT nephrotoxic? | Sirolimus |
| What is the most common use of Sirolimus? | Kidney transplant rejection prophylaxis specifically |
| Monoclonal antibody; blocks IL-2R. MOA of which immunosuppressant? | Basiliximab |
| What is the antimetabolite precursor of 6-mercaptopurine? | Azathioprine |
| How does Azathioprine works? | Inhibits lymphocyte proliferation by blocking nucleotide synthesis |
| What is the most common adverse effect of Azathioprine toxicity? | Pancytopenia |
| What drug, if coadministered with Azathioprine, can increase risk of toxicity? | Allopurinol |
| What is the MC use for Mycophenolate mofetil? | Lupus nephritis |
| What is the MOA of Mycophenolate Mofetil? | Reversibly inhibits IMP dehydrogenase, preventing purine synthesis of B and T cells. |
| What is common association of Mycophenolate mofetil? | Invasive CMV infection |
| What is the immunosuppressive role of Glucocorticoids? | Inhibit NF-kB; Suppress both B and T-cell function by decreases transcripo of many cytokines Induce T cell apoptosis |
| What level of transcription is halted by glucocorticoids? | Cytokine |
| Which kind of immunosuppressants are seen with NF-kB inhibition? | Glucocorticoids |
| What common bone-related adverse characteristic is seen in glucocorticoid toxicity? | Avascular necrosis (femoral head MC) |
| What causes the demargination of WBCs in glucocorticoid use? | Artificial leukocytosis |
| What is a risk of abruptly stopping glucocorticoids after chronic use? | Adrenal insufficiency |
| IMP dehydrogenase is inhibited by _______________________. | Mycophenolate |
| What enzyme is inhibited by 6-MP? | PRPP amidotransferase |
| What are some important cytokines that are involved in bone marrow stimulation? | Erythropoeitin, Colonny stimulating factors, and Thrombopoietin |
| What is an EPO agent? | Epoetin alfa |
| What is treated with Epoetin alfa? | Anemias (espicially in renal failure) |
| What common Colony stimulating factor agent? | Filgrastin (G-CSF), Sargramostim (GM-CSF) |
| What are the clinical uses of Colony stimulating factors? | Leukopenia |
| What are some thrombopoietin agents? | Romiplostim (TPO analog), Eltrombopag (TPO receptor agonist) |
| What agent is used to treat autoimmune thrombocytopenia? | Thrombopoietin |
| What is Aldesleukin? | IL-2 agent |
| What are the common uses of Aldesleukin? | Renal cell carcinoma, metastatic melanoma |
| What are the conditions treated with IFN-alpha? | Chronic Hep C and Hep B, and renal cell carcinoma |
| INF-beta is used to treat: | Multiple sclerosis |
| What immunotherapeutic agent is used to treat Multiple Sclerosis? | IFN-beta |
| Which interferon is used to treat Chronic granulomatous disease? | IFN-gamma |
| What is treated with IFN-g? | Chronic granulomatous disease |
| Which is the target of Alemtuzumab? | CD52 |
| Which monoclonal antibody immunosuppressive is directed against VEGF? | Bevacizumab |
| What are the main cancers treated with Bevacizumab? | Colorectal cancer, RCC, and non-small cell lung cancer |
| Cetuximab targets __________________. | EGFR |
| RItuximab targets? | CD20 |
| HER2 is targeted by with immunosuppressant? | Trastuzumab |
| Which are some soluble TNF-alpha monoclonal antibodies? | Adalimumab, infliximab, certolizumab |
| What is a decoy TNF-alpha receptor? | Etanercept |
| What conditions are treated with TNF-alpha monoclonal antibodies? | IBD, RA, ankylosing spondylitis, and psoriasis |
| Eculizumab is often used to treat ________________. | Paroxysmal nocturnal hemoglobinuria |
| What is used in relapsing multiple sclerosis? | Daclizumab |
| alpha4-integrin is the target of: | Natalizumab |
| What is a risk associated with Natalizumab? | PML in patients with JC virus |
| What is the target of Abciximab? | Platelet glycoprotein IIb/IIIa |
| What is the most common use of Abciximab? | Antiplatelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention |
| RANKL is targeted by ________________. | Denosumab |
| When is Denosumab used? | Osteoporosis; inhibits osteoclast maturation |
| Omalizumab targets? | IgE |
| What is the most common use for Omalizumab? | Refractory allergic asthma |
| What is the use for Palivizumab? | RSV prophylaxis in infants |
| RSV F protein is targeted by? | Palivizumab |
Created by:
rakomi
Popular USMLE sets