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Hypersensitivity Imm

WVSOM -- Immuno/Micro -- Hypersensitivity

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