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Hypersensitivity Imm
WVSOM -- Immuno/Micro -- Hypersensitivity
| Question | Answer |
|---|---|
| What is hypersensitivity? | inappropriate immune response that causes pathology |
| What are functional exceptions to hypersensitivity? | hypereosinophilia; hyper IgE syndrome; multple myeloma; genetic disorderst that manifest immunologically (not an immune response) |
| What is an inappropriate response ? | is when there is a response to a "non-combatant" that is more damaging than necessary |
| What are haptens? | molecules too small so they covalently bond to self proteins and make them look foreign |
| describe the immunologic mechanism of Th2 allergy? | Th2 is the default pathway to IgE production so if a problem exists it usually manifests there. Th2 signals B cells to produce more IgE than necessary after first exposure |
| what is atopy | affecting parts of teh body not in direct contact with teh allergen; not hyper-IgE syndrome; Atopy is specifically generated IgE antigen |
| What IL do Th2 release to promote B cells to release IgE | IL-4 and IL-13 |
| What are some genetic factors that affect Th2 allergy? | presence of HLA alleles; polymophisms of FaRI-b; polymorphisms of IL-4; polymorphism of CD 14 |
| What are some environmental factors that affect Th2 allergy? | allergen sensitization; having few sibling; excessive hygiene; receipt of antibiotics in first 2 years of life; vaccination adn prevention of disease |
| What triggers Th2 allergies? | viral infections; exposure to allergens; tobacco smoke; indoor and outdoor pollutants |
| What target organs have defects in Th2 allergies? | bronchial epithelium; skin; gut |
| What kind of antigen does IgE target? | soluble antigen |
| What is teh effector mechanism of Type I | mast-cell activation |
| What is the immune reactant in Type II reactions | IgG |
| What is the antigen in type II reactions? | Cell-matrix-associated antigen or cell-surface receptors |
| What is teh effector mechanism in Type II reactions? | complement (phagocytes, NK cells) and antibody alters signalling |
| What are some examples of type II hypersensitivity reactions | some drug allergies and chronic urticaria |
| What is the immune reactant for type III reactions? | IgG |
| What kind of antigen is affected with Tpye III reactions? | soluble antigen |
| What is teh effector mechanism with Type III reactions? | complement, phagocytes |
| What are some examples of hypersensitivity reactions? | serum sickness, arthus reactions |
| What are the immune reactants with type IV reactions? | Th1, Th2 and Cytotoxic T lympocytes |
| What is the antigen in Th1 and Th2 cell Type IV antigens? | soluble antigen |
| What is the antigen in Cytotoxic T Lymphocyte Type IV reactions? | cell-associated antigen |
| What is the effector mechanism with Th1 Type IV hypersensitivity reactions? | macrophage activation |
| What is teh effector mechanism with Th2 Type IV hypersensitivity reactions? | IgE production, Eosinophil activation, mastocytosis |
| What is teh effector mechanism with CTL Type IV hypersensitivity? | cytotoxicity |
| What is an example of Th1 cell Type IV hypersensitivty reaction? | contact dermatitis, tuberculin reaction |
| What is an example of Th2 cell Type IV hypersensitivity reaction? | chronic asthma, chronic allergic rhinitis |
| What is an example of CTL Type IV hypersenitivity reactions? | contact dermatitis |
| How is IgE made? | made by plasma cells after Th2 stimulation |
| When is IgE elevated | in atopic disease (54% of asthmatics) |
| What receptor does IgE bind to? | FceRI |
| What is the origen of mast cells and basophils? | bone marrow |
| Where are mucosal mast cells distributed? | gut, lungs and mucosa |
| What is the life span of mucosal MC? | < 40 days |
| Which mast cell has teh most histamine content? | connective tissue Mast Cells |
| What is the distribution of connective tissue MC? | ubiquitous |
| What is the lifespan of CT mast cells? | months to years |
| What is teh distribution of basophils? | blood |
| What is the life span of basophils? | 8-12 days |
| How many mast cells, basophils and eosinophils does it take for anaphylaxis? | 10% |
| Does IgE cross the placenta? | no |
| what does crosslinking of IgE to mast cells lead to? | degranulation |
| What is the most potent inducer of anaphylaxis? | antibodies to FcERI |
| Granules contain? | histamine, heparin, tryptase, chymase, carboxypeptidase |
| What do mast cells produce on stimulation? | leukotrienes, prostaglandins, PAF, cytokines adn chemotactic factors |
| What is type II hypersensitivity? | cytotoxic IgG |
| What is ADCC? | antibody dependent cell-mediated cytotoxicity |
| What is involved in type II hypersensitivity? | complement mediate cell lysis. |
| What cells are involved in type II hypersensitivity? | macrophages, neutrophils, eosinophils, and NK cells |
| What are the 2 types of complement mediate cell lysis | warm type and cold type |
| What is warm type complement mediate cell lysis | IgG extravascular hemolysis |
| What is cold type complement mediate cell lysis? | IgM intravascular hemolysis (full complement fixation |
| What are common Type II reactions? | transfusion reactions, hemolytic disease of the newborn and autoimmune hemolytic anema |
| What antibody is involved in transfusion reactions? | IgM |
| What causes autoimmune hemolytic anemia? | drug reactions |
| what is type III hypersensitivivity reaction? | immune complex. |
| What happens in immune complex formation? | zone of anti bodies in excess join to geter to form a zone of equivalence which is a large complex. a zone of antigen excess occurs with small complexes |
| Where is the site of reaction/deposition in type IV | blood vessels, skin, lung, kidney, skin |
| What kind of type III reaction is where the skin is exposed? | arthus reaction |
| What happens to the skin at the site of deposition in type III reactions? | petechia |
| What is an arthus reaction? | immune complex is formed in tissue outside the blood |
| Why is a type III reaction take so long? | normally don't get a first adn second exposure, but a rather long first exposure where antibodies are made adn then you react. Complement activation and numerous cells come into the area |
| What is a type III reaction where immune complexes are formed in the blood? | serum sickness |
| What happens in serum sickness | increaed vascular permeability; immune complexes activate inflammation in blood vessels. |
| what is the receptor in Type III serum sickness? | FcGRIII; low affinity receptor and becasue the threshold fo ractivation via this receptor is considerably higher than for the IgE receptor so the reaction is slow. |
| What are conditions that cause immune complex disease? | persistent infection, autoimmunity, inhaled antigen |
| In type III hypersensitivity explain the immune complexes that increase vascular permeability? | immune complexes aciavte inflammation in blood vessels. the FcyRIII and complement activation causes vascular permeability |
| That is type IV hypersensitivity? | delayed cellular |
| What is activated in TypeIV sensitivity? | actiavted T-cells (Th1 and Th2) and macrophages |
| Explain Type IV delayed type hyerpsensitivity? | T cells are activated by antigens on CD4 and 8. Cytokins are released adn macrophages release inflammatory mediators |
| What is the appearance of type IV delayed hypersensitivity by contact? | eczema |
| What is the appearance of tuberculin type IV hypersensitivity? | local induration |
| Waht is the appearance of a granuloma in type IV hypersensitivity? | hardening of the skin or lung |
| What is the antigen in granulomas? | persisiten antigen |
| What cells take up antigen in contact type IV hypersensitivity and where do they migrate? | langerhan's cells (APCs) and migrtate to T cells area of lymph nodes |
| What is the effected phase of type IV reactions? | second exposure to agent. actiavted t-cells are out there so antigen activates teh T cells again and takes it instead of using langenhan's cells |
| How do you diagnose Type I hypersensitivity? | skin test, "wheal and flare" |
| What is the response to allergic rhinitis? | irritation of nasal mucosa |
| what is teh response of anaphylaxis | edema, vasodilation, shock |
| Waht is the response to allergic asthma | bronchial constriction and airway inflammation |
| What is the response to wheal and flare | local edema adn local vasodilation |
| what is teh response to food allergy | vomiting, pruritus, diarrhea and urticaria |
| Waht is teh most ocmmon atopic hypersensitivity reaction? | allergic rhinitis |
| What is allergic rhinitis? | IgE mediated adn localized to thenasal mucosa an conjunctiva |
| What are lab findings are found in chronic rhinitis? | numerous eosinophils in nasal secretions and tissues. may have peripheral blood eosinophila |
| What are s/s in anaphylaxis? | sudden drop in BP; histamine and PAF respiratory symptoms; hypovolemic shock, wheezing and sypena; hypersecretion of mucus; crampy ABD pain |
| What are common substances known to cause anaphylaxis | lobster, shrimp, crab, clams, fish, peanut, sesame seeds, cottonseed, caraway seeds, peas adn beans, mustard seeds; insect venom; dander |
| What are some drugs known to cause anaphylaxis? | insulin ACTH vasopressin, parathormone, amphotericin B, trypisn, dextran, toxoids, PCN, strepotmycin, cephalosporin, tetracycline, vaccines, allergen extracts, barbituates, diazepam |
| Waht is the treatment for anaphylaxis? | epinephrine |
| What are some type II diseases? | goodpasture's sydrome, pemphigus, maysthenia gravis and type I diabetes (delayed onset) |
| What is goodpasture's syndrome? | anti-Glomular Basement Membrane found in kidney and lung |
| What is pemphigus? | anti-desmoglein 3; protein that binds cells togetehr; true dermalogical emergency; intraepidermal split |
| What is myasthenia gravis | autoantibodies tha blcok teh AChR (nicotinic) |
| What is affected with delayed onset of type I diabetes? | anti-islet antibodies |
| How do you diagnose type II diseases? | coomb's test (coagulation; immunohistolochemical stain and ELISA |
| what is a coomb's test | coagulation test; detects IgG anti-antibodys |
| What is treatment in type II hypersensitivity? | immunosuppressants; corticosteroids; intravenous IgG |
| What conditions cause Type III hypersensitivity | persistent infection; autoimmunity and inhaled antigen |
| How do you diagnose Type III hypersensitivities | granular anti-immunoglobulin immunofluorescence staining; examination of tissue biopsies for deposits of IgG and complement; |
| How do you treat type III hypersensitivity | alleviation of symptoms (NSAIDS); steroids and immunosuppressants; |
| What cels are seen in granulomas? | fibroblasts, connective tissue, macrophages, giatn cells, t cells |
| What happens in a granulomas? | has an outer rim of fibroblasts and collagen with a central area of coagulation necrosis |
| granulomous disease are caused by? | persistant antigens |
| What are some granulomatous disesases? | tuberculosis, leprosy, leishmaniasis, hydatid cyst, hisoplasma |
| What initiates a Type II reaction? | initiated by the binding of antibody to a cell membrane or to the extracellular matrix |
| What type of interaction is involved in a type III reaction? | interaction of antibodies with soluble molecules to make soluble antigen-antibody complexes which then become deposited in tissues |
| What are type IV reactions? | those in which cells of the immune system directly attack host cells in the absence of antibody. |
| Crosslinking of IgE on mast cells to allergens causes what? | mast cell degranulation that releases vasoactive amine, cytokines/chemokines and lipids |
| What does IgE rapidly bind to? | FcRe (cd23) on mast cells |
| What is the difference between FcRe and other FC receptors? | it only binds ti IgE. IgE will also bind to FcRe in the absence of antigen while other FcRs bind only antigen-bound antibody. |
| What happens in ADCC | FcR bearing cells (monocytes, neutrophils, eosinphoils, NK cess) bind to cells that have IgG or IgM bound to the surface epitopes |
| How is complement activated in Type II reactions? | IgM and IgG geneate C3b and C4b adn these are then dpositied on teh surfaces of antibody-coated cells to function as opsonins. |
| What antibody binding occurs in hemolytic anemia? | IgM antibodies bind to carbohydrate structures on erythrocytes resulting in their phagocytosis and in teh presence of coplement their rapid lysis. IgG binds to Rh factors in Erythrocytes |
| What part of blood cells to IgM bind to in blood group antibodies? | carbohydrate structures on erythrocytes (A/B) |
| What part of blood cells do IgG bind to in blood group antibodies? | Proteins of teh Rh factor |
| What is the interaction of antibody with teh exracellular matrix in type II reactions? | bind to the basement membrane and activate the classical pathway of complement geneating anaphylotoxins (C5a, C4a, C3a) that recruit neutrophils and monocytes. |
| What happens in localized reactions in type III reactions? | Arthus reactions; antibody diffuses from the vasculature to foem large immune precipitates that activate complement to induce painful localized edematous inflammatory lesions |
Created by:
tjamrose
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