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Hypersensitivity
| Question | Answer |
|---|---|
| Hypersensitivities | overreaction of immune system to Ags; d/t harmful tissue, systemic abnormalities, Ab-Ag rxn, allergic reactions |
| Type I Hypersensitivity | Ag bound to IgE Ab (bound to its Fc receptor on mast cells); humoral; immediate response |
| 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 |
| Type III Hypersensitivity | deposition of Ag-Ab immune complexes in tissues causing an inflammatory response that activates complement; humoral; immediate response |
| Type IV Hypersensitivity | caused by products of Ag-specific effector T cells; **this is the only cell-mediated hypersensitivity reaction**; delayed reaction |
| 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 |
| Fc-IgE binding to FceRI receptor | this is the strongest Ab-Fc receptor interaction; after |
| 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) |
| 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 |
| Major allergens | proteases ex: Cysteine protease from D. pteronyssinus is responsible for 20% of allergies |
| Cysteine protease | papai; related to papaya; commercial production results in sensitization of workers |
| Subtilisin | biological component in some laundry detergents |
| Chymopapain | related to papain; used to degrade IV discs in sciatica pts; can cause systemic anaphylaxis in those who are sensitized |
| 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 |
| 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) |
| Mast cells | reside in mucosal & epithelial tissues; alert immune system to local trauma & infection; form granules when they mature |
| 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 |
| 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) |
| Mast cells synthesize: | Chemokines, cytokines, leukotrienes, prostaglandin D2 |
| 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 |
| Prostaglandin D2 | dilates and increases permeability of blood vessels; chemoattractant for neutrophils |
| 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 |
| 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) |
| 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 |
| 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) |
| 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 |
| 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 |
| 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 |
| 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) |
| 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 |
| 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) |
| 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) |
| Hemolytic transfusion reactions | type II; rxn to preformed antibodies related to AB blood types; |
| 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+ |
| 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) |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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) |
| 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 |
| 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 |
| 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 |
| Treatment for serum sickness | antivenom antisera; mouse-anti-human T-cell antibodies used to prevent transplant rejection |
| Systemic Lupus Erythematosis | type III; kidney affected by Antinuclear antibodies (present on Immunofluorescence); C3 levels are usu decreased; leads kidney failure |
| 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); |
| 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 |
| Type IV: Lymphokines | Macrophage chemotaxin, Migration inhibitory factor, blastogenic factor, transfer factor |
| Migration inhibitory factor | type IV; keeps MQs from leaving site; ensures continuation of processing of Ag for T cells |
| Blastogenic factor | type IV; stimulates cell growth and lymphocyte blast transformation |
| Transfer factor | type IV; transfers Ag specificity; causes a resting T cell to become activated |
| 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) |
| 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) |
| 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 |
Created by:
bscaryp