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Hypersensitivity

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Answer
Hypersensitivities   overreaction of immune system to Ags; d/t harmful tissue, systemic abnormalities, Ab-Ag rxn, allergic reactions  
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Type I Hypersensitivity   Ag bound to IgE Ab (bound to its Fc receptor on mast cells); humoral; immediate response  
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Type II Hypersensitivity   small molecules bound to cell surface which modifies cell surface profile to look foreign to the body's immune system; humoral; immediate response  
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Type III Hypersensitivity   deposition of Ag-Ab immune complexes in tissues causing an inflammatory response that activates complement; humoral; immediate response  
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Type IV Hypersensitivity   caused by products of Ag-specific effector T cells; **this is the only cell-mediated hypersensitivity reaction**; delayed reaction  
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Type I: Ag makes contact & induces response   Ag processed by APC (ex: MQs) & is presented to Tcells; activated T cells produce cytokines that activate B cells to produce antibody; Mucous membranes are rich in B cells that produce IgE (& IgA) & mast cells  
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Fc-IgE binding to FceRI receptor   this is the strongest Ab-Fc receptor interaction; after  
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Cross-linking of the FceRI receptor   antigens can have repetitive epitopes or 2+ different epitopes; they crosslink with IgE molecules of the same or different specificities on a mast cell to cause instantaneous degranulation (histamine, inflam mediators)  
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Allergens that cause Type I reactions   small dried ptns from pollen, animal skin or saliva, dust mite feces; usu inhaled, caught in mucus & rehydrated so antigenic ptns are released & presented by APCs to CD4 Tcells to stimulate a TH2 response  
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Major allergens   proteases ex: Cysteine protease from D. pteronyssinus is responsible for 20% of allergies  
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Cysteine protease   papai; related to papaya; commercial production results in sensitization of workers  
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Subtilisin   biological component in some laundry detergents  
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Chymopapain   related to papain; used to degrade IV discs in sciatica pts; can cause systemic anaphylaxis in those who are sensitized  
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Type I: Initial exposure   24-48 hour waiting period for Ab to bind mast cell prior to Ag binding (Fc-Fab); leads to release of vasoactive chemicals  
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The FceRI receptors on mast cells, basophils and activated eosinophils differ from the Ag receptors on B and T cells   Ab binding results in immediate effector function & symptoms; AND individual cells are not restricted to a single antigenic specificity (no need for cell prolif/diff)  
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Mast cells   reside in mucosal & epithelial tissues; alert immune system to local trauma & infection; form granules when they mature  
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Mast cell granule contents   Histamine; binding to H1 receptors of endothelial cells induce vessel permeability, migration of cells/molec into allergen-containing tissue; causes inflammation; Binding to smooth muscle cells contracts/restricts airway; mucosal lining increases mucus  
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Other chemicals released from mast cell granules   chymotryptase, tryptase (they break down ECM); TNF-a (inc expression of adhesion molecules on endothelial cells for WBC infiltration)  
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Mast cells synthesize:   Chemokines, cytokines, leukotrienes, prostaglandin D2  
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Leukotrienes   similar activities to histamine, but more potent; allows for rapid response (gives time for leukotrienes to be produced); responsible for inflam, airway constriction, mucus secretion  
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Prostaglandin D2   dilates and increases permeability of blood vessels; chemoattractant for neutrophils  
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Eosinophils   1-4% of total WBCs; most live in tissues underlying epithelia of respiratory, GI and urogenital tracts; w/Ag stimulation, TH2 cells are activated releasing cytokines to stimulate inc production & activate endothelial cells/monocytes to attract these cells  
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Eosinophils during an inflammatory response   must be induced to express FceRI and Fcgamma receptors; they can cause tissue damage (ex: IL-5 induced heart damage in Tcell lymphoma & airway damage in chronic asthma)  
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Basophils   related to eosinophils; defense against parasitic infections; reciprocally regulated w/eosinophils; present as <1% of WBC pop; recruited into sites of allergic reactions; dark granules cover nucleus  
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Mast cells, eosinophils & basophils interact during allergic response   mast cells degranulate (release mediators for inflammatory response that recurits eosinophils/basophils); Eosinophils degranulate (release major basic protein causing mast cell/basophil degranulation)  
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Allergic Rhinitis   d/t inhaled allergen; "hay fever" allergens diffuse thru nasal mucosa & activate mast cells; local edema blocks airways, mucus has eosinophils, histamine irritates nose; can spread to ears/throat/sinuses (bacterial infxn?); conjunctiva is sensitive too  
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Allergic Asthma: type I   allergens activate submucosal mast cells in LRT; degranulation causes fluid/mucus secretion & bronchial constriction; chronic inflam d/t TH2 cells, eosin, PMNs; air trapped in lungs makes breathing difficult  
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Wheal and flare: type I   Immediate rxn: IgE-med release of mast cell granules; localized to skin in 5-15min; late phase reaction occurs 6-8hrs after immediate rxn d/t leukotrienes, chemokines, cytokines from mast cell  
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Generalized anaphylaxis: type I   Ag enters bloodstream; loss of fluid from vessels causes swelling/drop in bp/shock; can be fatal w/in minutes (bees, peanuts, PCN)  
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Allergy shots   IgE is a cytophilic molecule which has affinity for cell membranes; shots attempt to desensitize pt by producing IgG that will instead bind to the allergens so it will be removed before IgE can find it  
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Type I Symptoms/Causes   Dilated vessels (erythema; if widespread causes shock); Inc capillary permeability (local edema; can drop bp); Bronchial constriction (wheezing/coughing); Mucus (congestion); Stimulate nerve endings (iching, pain)  
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Type II Hypersensitivity   cytotoxic reactions; IgG & IgM mediated w/ or w/o complement activation; Ab are directed against fixed tissue antigens & damages tissues (complement cell lysis (C3, C3a, C5a), platelet destruction)  
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Hemolytic transfusion reactions   type II; rxn to preformed antibodies related to AB blood types;  
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Hemolytic disease of the newborn (HDN)   typeII: Rh(-) mom, Rh(+) baby; mom is sensitized by 1st pregnancy; IgG antibodies are produced & can cross placental barrier if next child is Rh+  
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ABO incompatibility of HDN   less severe & more common; no previous pregnancy is necessary; some women have IgG anti-A or B (usu occurs when mom is type O and baby is either A or B)  
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Hemolytic anemias   type II; can be side effects of drugs; drugs bind surface of RBC & new epitopes alert the immune system (ex: PCN, quinidine, methyldopa); IgM and IgG are produced in response to drug-cell conjugates  
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Natural Killer Cells   a/w type II hypersensitivity; Ab-dependent cell toxicity; this subclass of cytotoxic Tcells target cell destruction; IgG attach target cells & NK w/those IgG receptors will attach form Ab-cell complex & destroy cell  
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Goodpastures Syndrome   type II; IgG Ab formed against type IV collagen (specific to BM); Ab deposits mostly in renal glomeruli/tubules (impair fxn & lead to failure); also present in lungs  
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Autoimmune Thrombocytopenia Purpura   type II; autoantibodies against platelets; **easy bruising & bleeding gums*; platelets: 20-50,000 (nml: 150-450,000); Severe: spontaneous stomach bleeding, intracerebral hemorrhage  
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Graves Disease   type II; diffuse goiter, thyrotoxicosis, opthalmopathy, hyperthyroidsim; Ab against TSH receptors (behave as thyroid stimulants & compete for receptor); Negative feedback is altered b/c TSH can't bind  
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Graves Disease: Symptoms and Treatment   irritability, wt loss; insomnia; protrusion of eyes; Medicate to reduce thyroid hormine levels, Surgically remove all or part of gland, or radiate with radioactive iodine  
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Myastenia Gravis   type II; autoantibodies against alpha chain of nicotinic ACh receptor at NMJ; promotes internalization/degradation of ACh receptors & blocks NM transmission; progressive dx (can be fatal; ocular motor; Generalized: trunk, arms, legs)  
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Type III Hypersensitivity   immune complexes (Ab-Ag-complement adhere to Fc receptors on phagocytes) deposit anywhere in host tissues; Humoral & Cellular factors accumulate at site; excess Ab can allow complexes to stay in blood; Complement attracts PMNs for inflam/protease damage  
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Size of type III immune complexes   usu variable; large ones activate complement efficiently & are ingested by phagocytes; Smaller complexes must circulate until deposited in vessel wall & accumulate of smaller ones activate comp, C3a-mast cell degran; C5a - recruits WBCs); clots form  
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Serum Sickness   type III; systemic disorder d/t injection of foreign serum containing Ab to a disease caused by microbes (horse or other animal); Ab form against foriegn ptns, complex & deposit in tissue; red nasty lesions are on lower extremities/tissues destroyed  
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Treatment for serum sickness   antivenom antisera; mouse-anti-human T-cell antibodies used to prevent transplant rejection  
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Systemic Lupus Erythematosis   type III; kidney affected by Antinuclear antibodies (present on Immunofluorescence); C3 levels are usu decreased; leads kidney failure  
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Type IV hypersensitivities   delayed; **NO HUMORAL ABs**; prototype for this reaction is Koch's TB skin test phenomenon (2nd exposure has delayed rxn of 48-72hrs);  
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Type IV immune response   mediated by Th1 cells that recognized Ag presented by MHCII; Mononuclear cell infiltration (sensitized lymphocytes migrate, blast transform, & proliferate); Lymphokine secretion affect other cells  
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Type IV: Lymphokines   Macrophage chemotaxin, Migration inhibitory factor, blastogenic factor, transfer factor  
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Migration inhibitory factor   type IV; keeps MQs from leaving site; ensures continuation of processing of Ag for T cells  
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Blastogenic factor   type IV; stimulates cell growth and lymphocyte blast transformation  
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Transfer factor   type IV; transfers Ag specificity; causes a resting T cell to become activated  
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Differences between immediate and (delayed) sensitivity   seconds-min skin rxn (48-72hrs); Passive serum transfer (T-cells); PMNs, mast cells (Mononuclear cells/lymphocytes); Histamine, seratonin, kinins (Lymphokines); Desensitization (no desensitization)  
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Type IV Sensitivity: Clinical findings   delayed skin rxn (ex: TB skin test); a positive rxn meas pt has previously been sensitized; Contact Dermatitis (allergens including poison ivy, poison oak, soaps, cosmetics)  
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Poison Ivy   type IV; penetrates the skin & bonds w/extracellular ptns (skin MQs & langerhan cells make antigenic peptide & present via MCHII to TH1 cells); Chemicals that penetrate plasma membranes can alter intracellular ptns & present to CD8 cells via MHCI molecule  
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