Immunology 24 - Immunology 24- Autoimmunity Autoimmune...

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Immunology 24- Autoimmunity Autoimmune diseases Broadly classified as “systemic” or “organ-specific”; depends on immune mechanism responsible Possible to have more than one disease Oran specific= type I diabetes, Goodpasture’s syndrome, multiple sclerosis/Crohns disease/ psoriasis, Graves disease/Hashimoto’s thyroiditis/autoimmune haemolytic anemia/autoimmune Addison’s disease/ Vitiligo/Myasthenia gravis Systemic specific= rheumatoid arthritis, sclerodoma, systemic lupus erythematosus/Primary Sjogren’s syndrome/polymyositis Ones grouped together have similar regulator mechanisms Type I hypersensitivity reactions not really associated with autoimmune diseases Systemic autoimmunity Type III hypersensitivity; immune complex mediated disease; complement and FcR Rheumatoid factor= antibody against Ig (antibody against antibody) Syndrome= Rheumatoid Arthritis Autoantigen= rheumatoid factor IgG complexes (targeted towards joints= swollen knuckles, deviation of fingers) Consequence= arthritis Autoantigens in SLE and related diseases SLE= associated with a broad range of autoantigens (DNA, RNA, IgG); normally the antigens are constricted inside a cell but get released as tissue is destroyed Systemic Lupus Erythematosus (SLE): Type III hypersensitivity; immune complex mediated disease; become deposited on small blood vessel walls→ complement and FcR mediated tissue destruction Tissues affected= kidneys (most problematic), skin, muscles, joints, lungs, heart, brain **butterfly rash Tissue Specific Autoimmunity Type II hypersensitivity; IgG against cell surface antigen; cell destruction (via complement or FcR); alteration of signalling or function (receptor blockade or activation) Syndrome= autoimmune haemolytic anemia (type II hypersensitivity) Autoantigen= Rh blood group antigens, I antigen Consequences= destruction of RBCs by complement and FcR+ phagocytes; anemia RBC are coated with IgG autoantibodies which bind to cell-surface antigen and are rapidly cleared from circulation by uptake by Fc receptor-bearing macrophages in the fixed mononuclear phagocytic system; RBCs coated with IgM autoantibodies fix C3 and are cleared by CR1 and CR3 bearing macrophages in the fixed mononuclear phagocytic system; uptake and clearance by these mechanisms occurs mainly in the spleen; the binding of certain rare autoantibodies that fix complement extremely efficiently causes the formation of the membrane-attack complex on the RBCs, leading to intravascular hemolysis Systemic/Tissue specific autoimmunity Type II hypersensitivity
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Ab directed against cell surface receptors= interfere with signalling (block or activate) ; ex. Chronic urticaria (antibody against FcERI alpha chain) Autoimmune haemolytic anemia, autoimmune thrombocytopenic purpura, goodpasture’s syndrome, pemphigus vulgaris, acute rheumatic fever Graves Disease Type II hypersensitivity Antibodies to receptor for thyroid stimulating hormone (agonist activity)= increase
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This note was uploaded on 02/08/2012 for the course PATHOLOGY 3245 taught by Professor X during the Spring '11 term at UWO.

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Immunology 24 - Immunology 24- Autoimmunity Autoimmune...

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