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Transcript
Immune Hypersensitivity Chapter 18 Self-Test Questions: Intro: all A1-2: all A3: 1, 3, 5 A4: all B: 1, 2, 4, 5 C: 1 - 4 D: 1 - 4 Hypersensitivities 1 What characteristics are shared by all hypersensitivies? Immune responses: Primary (sensitization) response Secondary (activation) response Abnormal (hyper-) response to antigens (allergens) Symptoms: localized or systemic Onset can be: Early, Late or Chronic Hypersensitivities 2 What are hypersensitivities? 4 types of hypersensitivities (Gel and Combs classification) Immune Name system involved Effectors Type 1 “Atopic” Humoral (IgE) mast cells eosinophils Effects inflammation (anaphylaxsis) Onset seconds Type II “Cytotoxic” Humoral/ Complement macrophages complement cell destruction (hemolysis) hours Type III “Im. Complex” Humoral/ Complement granulocytes inflammation hours Type IV “Delayed type” Cell-mediated -- TH1 macrophages inflammation days Hypersensitivities 3 Type I – Atopic hypersensitivities AG presentation DCs, even Basos & Eosinos activate TH2 cells IgE production class switching to IgE Mast cell sensitization IgE binding to Fc receptors Mast cell activation Degranulation secretion synthesis Early phase & late phase responses McGraw-Hill Type-I Hypersensitivities 4 Early phase responses Molecular Mediators: Primary – in granules Secondary – synthesized later (w/in 1- few minutes) Localized clinical response (Atopy) atopic asthma: urticaria (hives) eczema (skin lesions) atopic rhinitis food allergies Systemic clinical response (anaphylaxis) anaphylatic shock Hypersensitivities 5 Late phase responses -- 4-6 hours later e.g., Erythema, etc “peak flow rate” measurements Due to: Early phase Late phase -- Cytokines from mast cells -- Recruited eosinophils & TH2 -- degranulation Chronic Type I -- eosinophilia -- inflammation: damaged airways & mucous membranes Hypersensitivities 6 What factors affect predisposition toward Type I hypersensitivities? Genetic factors Environmental factors Hygiene hypothesis Hypersensitivities 7 Treatment Skin testing -- carries some risk Drugs therapies -- Theophylline (blocks degranulation) -- antihistamines (block histamine receptors) -- epinephrine (reverses trachael & bronchiole SM and contracts arteriole SM) Desensitization Therapy Desensitization Hypersensitivities 8 Type II hypersensitivity -- “Cytotoxic” Ig binding to AG on cells -- triggers cell lysis Complement mediated Macrophage mediated Various types of hemolytic disorders e.g., Blood transfusion incompatibility {see section in chapter 17} Autoimmune disorders e.g.. Goodpasture’s syndrome RBC being phagocytosed in fetal erythroblastosis 1967 Science 158: cover Hypersensitivities 9 Type III hypersensitivity -- “immune complex” Localized: (Arthus reaction) -- could result from an insect bite 1) Ag-Ab complex Excess AG small complexes complement activation 2) mast cell degranulation 3) neutrophil recruitment 4) Triggering of inflammation C3a, C5a Systemic: Serum sickness Vasculitis Hypersensity pneumonitis -- Pigeon breeders disease (pigeon feces dust) -- Farmers lung (Actinomycetes) -- Mushroom picker’s… -- Cheese washer’s… -- Chicken plucker’s… -- etc., … disease Type III Hyper Hypersensitivities Adapted from Majno and Joris, 2004, Cells, Tissues and Disease 10 Type IV hypersensitivity “Delayed-type” -- slow onset ~day(s) (if sensitized) TH1-cell mediated Sensitization phase -- week(s) onset -- TH1 expansion Effector stage – day(s) onset -- TH1 & macrophage activation -- inflammation Latex type IV hypersensitivity Hypersensitivities 11 Type IV hypersensitivities, con’t Contact dermatis reactions Often involves hapten production e.g. to: hair sprays, plant toxins, turpentine TH1 Hypersensitivities 12 Tuberculosis (see Chapter 14 pp 212-213) -- Persistent Mycobacterium tuberculosis Granuloma (tubercule) formation TH1 cells and activated macrophages ‘caseous’ regions extended tissue destruction Hypersensitivities 13