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HYPERSENSITIVITY REACTIONS Innocous materials can cause hypersensitivity in certain individuals unwanted inflammation damaged cells and tissues Non-proper reaction of the immune system to foreign substances Mainly harmless substances after second or multiple times The effector mechanisms and tissue destruction in hypersensitivity reactions are identical to those seen in autoimmune diseases. ANTIBODY MEDIATED HYPERSENSITIVITY REACTIONS IgE Mast cell IgG immune complex FcR+ cells NK, macrophage IgG immune complex FcR+ cells Complement Hay fever Asthma Systemic anaphylaxis Certain drug allergies (penicillin) Serum sickness Arthus reaction 1-2 min4-8 h 2-8 h Type II hypersensitivity IgG type antibodies bound to the cell surface or to tissue antigens cells expressing the antigen become sensitive to complement mediated lysis or to opsonized phagocytosis frustrated phagocytosiss tissue demage the antibody inhibits or stimulates target cell function no tissue damage (e.g. M. gravis receptor blocker antibodies) MECHANISMS OF TYPE II HYPERSENSITIVITY REACTIONS Hemolytic anemia of newborns Erythroblastosis fetalis Drug induced Hemolytic anemia Trombocytopenia Penicillin-based antibiotics Anti-arythmic drug quinidin Myastenia gravis Penicillin-induced hypersensitivity The tissue, which can not be phagocytosed, is damaged Absorbed antigen (drug) FRUSTRATED PHAGOCYTOSIS MEDIATED BY IgG TYPE ANTIBODIES Binding Opsonization Internalization Enzyme release Opsonized surface Binding Frustrated Enzyme release phagocytosis TYPE III HYPERSENSITIVITY Antibodies binding to soluble antigens Small circulating immune complexes Depends on: Size of immune complexes Antigen-antibody ratio Affinity of antibody Isotype of antibody Size of immune complexes formed during immune responses The pathology is determined by the site of immune complex deposition Arthus reaction hard swelling, erythema THE PROCESS OF TISSUE DAMAGE CAUSED BY IMMUNE COMPLEXES Immune complexes activate the complement system, neutrophils, bazophil granulocytes and thrombocytes Blood vessel wall permeability Frustrated phagocytosis Serum sickness Mechanisms of tissue demage is independent on the site of deposition Steps of tissue demage Formation immune complexes in the blood Deposition depends on the size, composition and cytophylic properties of the antibody (IgM, IgG, IgA) FcRIII has a pivotal role Permeability of endothelium Tissue demage Increased permeability of blood vessels Reqruitment of neutrophils enzymes, chemoattractans, dilatators, prostaglandins fibrosis Consequences of tissue demage depends on the site of deposition Acute serum disease 7 10 days Polyclonal antibodies against snake venom produced in horses Immune suppresszive anti-lymphocyte globulin Bacterial trombolytic streptokinase treatment of miocardial infarction Subacute bacterial endocarditis pathogens are not eliminated Chronic viral hepatitis Serum therapy against diphtheria Corynebacterium diphtheriae Klebs-Lffler bacillus (1883) Edwin Klebs Emil von Behring Nobel prize 1901 Tom (1894, London) Skin symptoms of serum sickness Serum sickness TYPE IV HYPERSENSITIVITY REACTION T CELL MEDIATED PROCESS Type IV hypersensitivity reaction Chemokines, cytokines, cytotoxins Tuberculin skin test Ag = antigen Mycobacterium protein (PPD) Introduction of Ag Delayed-type hypersensitivity (DTH) (e.g., tuberculin skin test) T H 1 from a previous immunization (memory) *a contact-sensitizing agent is usually a small molecule that penetrates the skin then binds to self-proteins, making them look foreign Contact Dermatitis Delayed-type hypersensitivity is mediated by T cells

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