453405
Description
Flashcards by littlebluechair, updated more than 1 year ago
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Created by littlebluechair
almost 11 years ago
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| Question | Answer |
| Secretes interleukin (IL-1) to promote T cell activity | Macrophage |
| Expresses high levels of major histocompatibility complex (MHC) class 2 on its cell membrane | Macrophage |
| Macrophage precursor | Monocyte |
| Total levels and concentration of this antibody can be estimated using radioimmunoabsorbent test (RIST) and radioallergosorbent test (RAST) | IgE |
| What term is used to describe the portion of a molecule that serves as an antigen determinant? | Epitope |
| Type 1 reactions involve both primary and secondary mediators. Explain the difference between the two | Primary mediators: preformed molecules stored in granules that are directly released. Secondary mediators: generated de novo as a consequence of mast cell/basophil activation. |
| Histamine and proteases/hydrolases are primary mediators. What are their functions? | Histamine: vasodilation, increases vascular permeability and plasma leak (edema formation), smooth muscle contraction increases secretions (nasal, respiratory) Proteases/hydrolases: tissue damage, activate complement, cleavage of membrane receptors. |
| Leukotrienes B4, C4, D4, and E4 and cytokines are secondary mediators. What are their functions? | Leukotrienes: B4 -> recruits white blood cell (WBC). C4/D4/T4 -> vasodilation, increases vascular permeability. Cytokines: mediate the inflammatory response of the late phase |
| What are the two phases of type I hypersensitivity reactions? | Immediate phase: rapid degranulation of performed mediators in mast cells/basophils within minutes of reexposure to antigen that cross-links the cell-bound IgE. Late phase: 2 to 48 hours after antigen exposure; secondary mediators cause an influx, maturation and activation of inflammatory cells and increase their survival in tissue. |
| What are the symptoms of the immediate phase of type 1 reactions? | Edema, erythema, wheal and flare reaction in the skin, itching (skin, eye, nose), runny nose, wheezing. |
| What are the symptoms of the late phase of type I reactions? | Edema and induration (firmness due to increased tissue density), wheezing |
| What are the common clinical manifestations of type I hypersensitivity reactions? | Skin: urticarcia (hives), eczema Airways: rhinitis, asthma Eyes: Conjunctivitis |
| What are the consequences of IgE mediated responses in the gastrointestinal (GI) tract, airways and blood vessels? | GI tract: Increased fluid secretion, increased peristalsis -> expulsion of GI tract contents (diarrhea, vomitting) Airways: decreased diameter, increased mucus secretion -> expulsion of contents (phlegm, coughing) Blood vessels: increased blood flow, increased permeability -> edema, inflammation, and increased lymph flow takes antigen to lymph nodes |
| What is the most severe form of type I hypersensitivity reactions? | Systemic anaphylaxis, which manifests as life-threatening bronchoconstriction and systemic vasodilation (eg hypotensive shock) |
| What are some common cause of anaphylaxis | Peanut, bee venom, drug and latex allergy |
| What drugs are commonly given to prevent anaphylactic reactions? | Antihistamines, corticosteroids, and cromolyn sodium. Epinephrine can be given as treatment for anaphylactic reactions |
| How does cromolyn sodium work on mast cells? | It stabilizes mast cell membranes preventing degranulation |
| What do patients with atopic disorders (asthma, eczema and urticarcia) have elevated levels of? | IgE, Th2 cytokines |
| Drugs commonly cause hypersensitivity reactions by acting as haptens. What is a hapten and how does this induce hypersensitivity reactions? | A hapten is a molecule, which by itself cannot induce an immune response. The hapten, usually a drug of its metabolite, binds to an endogenous protein that then induces antibody formation. The antibody reacts to the hapten (drug or its metabolite) upon subsequent exposure. |
| What are type 2 hypersensitivity reactions also known as? | Cytotoxic hypersensitivity |
| What reaction occurs in type 2 hypersensitivity? | Antibodies against endogenous ell membrane antigens fix complement causing complement mediated lysis via membrane attack complex |
| For each disease associated with type 2 hypersensitivity, name the target: | . |
| Warm/cold autoimmune hemolytic anemia | Self-RBC membrane proteins (warm IgG, cold IgM) |
| Erythroblastosis fetalis | Fetal D-Rh antigen |
| Pernicious anemia | Intrinsic factor (binds B12) |
| Antineutrophil cytoplasmic antibodies (ANCA) vasculitis | Neutrophil granule proteins |
| C-Anca | PR3 |
| P-ANCA | Myeloperoxidase |
| Goodpasture syndrome | Alveolar and glomerular basement membranes |
| Rheumatic fever | Myocardial antigens that cross-react with streptococcal antigens (possibly the Streptococcus M protein) |
| Graves disease | Thyroid-stimulating hormone (TSH) receptor |
| Myasthenia gravis | Acetylcholine receptor |
| Lambert-Eaton myasthenic syndrome | Presynaptic Ca2+ channels |
| Pemphigus vulgaris | Epidermal desmosomes |
| Bullous pemphigpoid | Epidermal-dermal hemi-desmosomes |
| What drugs are associated with warm autoimmune hemolytic anemia? Of these, which drug (s) are associated with haptens? Which drug (s) generate autoantibodies? | Penicillin and quinidine are hapten forming. a-Methyl dopa generates autoantibodies |
| What test is positive in warm autoantibody disease? | Direct antiglobulin (Coombs) test |
| Cold autoimmune hemolytic disease has an acute and chronic form. What infections are associated with the acute form? What type of neoplasm is associated with the chronic form? | Acute form is associated with Mycoplasma pneumoniae and infectious mononucleosis (Epstein-Barr virus). Chronic form is associated with lymphoid neoplasms. |
| How is autoantibody is Grave disease different from other autoantibodies? | The autoantibody in Grave disease, a thyroid-stimulating immunoglobulin (TSI), actually binds and activates the TSH receptor. |
| What type 2 disease is mediated by an autoantibody that shares the same target as exfoliatin (Staphylococcus toxin in scaled skin syndrome) ? | Pemphigus vulgaris |
| What region of the autoantibodies attaches to the antigen in type 2 reactions? What region binds the complement? | IgG or IgM attaches to the antigen at their Fab region and attaches complement at their Fc region. |
| What are type 3 hypersensitivity reactions also known as? | Immune complex hypersensitivity |
| In type 3 reaction, formation of large antigen-antibody immune complexes deposit into tissues and fix complement. How does activation of complement result in tissue damage? How does this differ from type 2 hypersensitivity? | Complement activation recruits neutrophils, which release proteolytic enzymes and cause tissue damage. This differs from type 2 hypersensitivity in which tissue damage is caused by autoantibody-mediated complement activation (not by formation of large immune complexes) |
| One important factor that determines if antigen-antibody complexes deposit into tissue is the relative amount of antigen versus antibody. Why do antigen-predominant complexes typically form pathogenic deposits? | Antigen-antibody complexes are cleared when mononuclear phagocytes bind to antibody, resulting in endocytosis of the complex. In antigen-predominant complexes, fewer antibodies means less clearance and a propensity to form pathogenic deposits. |
| What is a pathology term used to describe type 3 inflammation in vessels? | Fibrinoid necrosis (eosinophilic staining accumulation) |
| What are the two typical type 3 hypersensitivity reactions? | 1) Arthus reaction: local deposition of immune complexes 2. Serum sickness: systemic inflammatory response to immune complexes deposits throughout the body. |
| Describe how an Arthus reaction is evoked: | Antigen is subcutaneously injected into a host with preformed antibodies to this antigen causing local edema and possible ulceration. |
| Hypersensitivity pneumonitis (farmer lung) is an Arthus reaction caused by inhalation of what bacteria? | Thermophilic actinomycetes |
| What is the typical clinical presentation of serum sickness? | Fever, hives, arthralgia, lymphadenopathy, splenomegaly and eosinophilia appear days to weeks after antigen exposure. |
| What drug is associated with serum sickness? | Penicillin. Note that penicillin can cause type I, II and III via hapten formation. |
| What re well-known disease that are resulted from type 3 immune complex deposition? | Poststreptococcal glomeruloneprhitis, rheumatoid arthritis, and systemic lupus erythematosus. |
| What are type IV hypersensitivity reactions also known as? | Delayed type hypersensitivity |
| What are the two types of type IV hypersensitivity? | Classic (tuberculin-like) DTH Contact dermatitis |
| In the first step of classic dth, macrophages present antigens to CD4+ helper cells and induce CD4+ cells to become what specific subtype? What cytokine secreted by macrophages drives this process? | Macrophages induce CD4+ T cells to mature into Th1 cells. IL-12 is the cytokine that drives this process. |
| These Th1 cells often remains in the circulatory system as memory cells. When the body is exposed to the antigen for a subsequent time, what cells do these Th1 cells activate? What cytokine secreted by the Th1 cells drives this process? | Th1 cells activate macrophages. y-IFN is the cytokine that drives this process. |
| What functions are enhanced when a macrophage is activated? | Increased phagocytosis, increased antimicrobial potency, increased antigen presentation, and further induction of inflammation. |
| What is seen histopathologically in classic DTH? | Granuloma: central core of epithelioid cells (type of y-IFN activated macrophages) with a rim of lymphocytes |
| What pathogens trigger classic DTH? | Mycobacteria and fungi |
| A positive tuberculin skin test is a classic DTH. Describe how a positive test presents | Minimal change in the first few hours followed by erythema and in duration of 48 to 72 hours. |
| How does contact dermatitis differ from classic DTH? | In contact dermatitis, previously sensitized Th1 cells enter the dermis and cause cytokine-mediated cell necrosis as opposed to the granulomatous reactions seen in classic DTH. |
| What are common contact allergens? | Plants (poison ivy/oak), chemicals, soaps, jewelry metal, topical drugs. |
| What are the common symptoms of contact dermatitis? | Erythema, pruritus, and necrosis of skin with formation of large blisters within 24 hours. |
| What is the role of MHC class 2 proteins on donor cells in graft rejection? | Recognized by helper T cells of the host -> proliferation, cytokine production and help to activate cytotoxic T cells to kill the donor cells. |
| What are the immunological contraindications to organ transplantation? | ABO blood group incompatibility, presence of preformed human leukocyte antigen (HLA) antibodies in the recipient's serum. |
| What does a lymphocyte cross-match do? | Screens for recipient anti-HLA antibodies against donor lymphocytes |
| What are the typical mechanisms by which transplant recipients are presensitized to donor antigens | Pregnancy, previous transplantation, blood transfusion |
| The two types of immunity are innate and adaptive immunity. What cells mediate innate immunity? | Monocytes/macrophages, neutrophils, natural killer (NK) cells, gamma-delta T cells. |
| Adaptive immunity is composed of two responses. What cells mediate each response? | Humoral immunity is mediated by B lymphocytes. Cell mediated immunity is mediated by T lymphocytes (also macrophages, NK cells) |
| B and T cell proliferation in early lymphocyte maturation is stimulated by which cytokine? | Interleukin 7 (IL-7) |
| What interacts with the T-cell receptor (TCR) of an immature, double-positive T cell (CD4+/CD8+) to signal differentiation into a single positive cell? In what organ does this occur? | Interaction with either major histocompatibility complex 1 (MHC 1) (CD8+) or MHC2 (CD4+) in the cortex of the thymus |
| What two processes eliminate immature T cells lacking proper antigen receptor specificities? | Positive selection selects for lymphocytes with TCRs that recognize self-MHC proteins, ensuring that only T cells with TCR that recognize MHC mature 2. Negative selection eliminates autoreactive t cells that bind to MHC with high affinity. |
| What mechanism drives cell elimination in positive selection? | T cells that cannot bind to self-MHC molecules undergo apoptosis. |
| Apoptosis of T helper cells (CD4+, Th) or cytotoxic T cells (CD8+, Tc) bearing TCRs for self-proteins is the result of what process? | Tolerance, which prevents autoimmune reactions. |
| What cytokine released by activated Th further stimulates Th-cell survival/proliferation? | IL-2. It binds to the IL-2 receptor on Th cells causing further proliferation. |
| Name the two signals that are needed to activate T cells | The first signal is the MHC/antigen complex interaction with a TCR specific for that antigen. The second is costimulatory signal of the CD28 protein on the T cell with the B7 protein on the antigen-presenting cells (APCs) |
| What is the result of an interaction between a T cell and an APC in the absence of costimulation? | Anergy or unresponsiveness of T cells. |
| What T cell protein displaces CD28 from B7, inhibiting T cell activation and ensuring T cell homeostasis? | Cytotoxic T lymphocyte antigen 4 (CTLA-4) |
| What is a consequence to T cells that lack CTLA-4? | It is thought that cells without CTLA-4 participate more often in autoimmune processes. |
| Which MHC class molecule presents processed antigens from organisms that have been phagocytosed? What cells possess this MHC class? | MHC-2 complexes on professional APC present extracellular, phagocytosed proteins to Th cells. |
| What cells function as professional APCs? | Dendritic cells, macrophages and B cells. |
| What is the source of antigen presented by MHC-1 molecules? What cells possess this class? | MHC-1 complexes on all nucleated cells present intracellular proteins to the Tc cells. |
| What is the cluster of polypeptides present in all T cells that is important in signal transduction by the TCR? | The CD3 complex |
| Induction of which of the T-cell helper lines (Th1 or Th2) elicits a more effective response against intracellular pathogens such as Mycobacterium tuberculosis? | Th1 cells are more effective against intracellular pathogens. |
| Which cytokine released by Th1 cells is involved in macrophage activation? | y-Interferon |
| What other signaling pathway results in macrophage activation? | The interaction of CD40 on macrophages with CD40L on T cells. |
| What transcription factor is involved in both y-interferon and CD40/CD40L signaling? | Nuclear factor kB |
| How do macrophages respond to y-interferon and CD40/CD40L signalling? | Cytokine release, increased microbicidal activity, increased phagocytic activity (through upregulation of B7 and MHC 2) |
| Once activated, what are the major cytokines released by macrophages? | Tumor necrosis factor (TNF), IL-1 and IL-8, leukocyte recruitment, IL-6, lymphocyte activation and IL-12, Th1 differentiation. |
| What are the microbicidal substances produced by activated macrophages? | Reactive oxygen species, nitric oxide and lysosomal enzymes |
| Total levels and concentration of this antibody can be estimated using radioimmunosorbent test (RIST) and radioallergosorbent test (RAST) | IgE |
| What term is used to describe the portion of a molecule that serve as an antigenic determinant? | Epitope |
| What term is used to describe a small molecule that can serve as an antigenic determinant only if it is attached to a large carrier molecule? | Hapten |
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