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Transcript
Immunopathology Dr JG Lawrenson Immunopathology • Hypersensitivity • Autoimmunity • Immunodeficiency © Dr JG Lawrenson 2001 Hypersensitivity • Hypersensitivity reactions are exaggerated or inappropriate immune responses that lead to tissue damage • Four types of hypersensitivity reaction are recognised: Type I, II, III and IV © Dr JG Lawrenson 2001 Type I Hypersensitivity • Type I (immediate type) reactions include: asthma, hay fever, food allergy • Also referred to as atopy • Triggered within minutes of exposure to a variety of environmental antigens e.g. pollen, house dust mite • Strong genetic link • Caused by an overproduction of IgE © Dr JG Lawrenson 2001 Type I Mechanism • Mast cells display a high affinity receptor for IgE • IgE is synthesised in response to certain antigens (allergens) • Allergens are deposited on mucous membranes and taken up and processed by antigen presenting cells (e.g. Dendritic cells or B cells) © Dr JG Lawrenson 2001 Type I Mechanism • Allergen presented to TH2 cells which provide cytokine signals to B cells to produce IgE Ig E binds to mast cells • Cross linking of IgE by subsequent exposure to allergen causes mast cell degranulation © Dr JG Lawrenson 2001 Type I Mechanism • Mast cell degranulation is the major initiation of the acute allergic reaction • Mast cell mediators include histamine, heparin and other factors • These cause, mucus secretion, vasodilation and oedema © Dr JG Lawrenson 2001 © Dr JG Lawrenson 2001 Mast cell mediators • Mast cell mediators include pre-formed and newly formed mediators • Pre-formed mediators include : histamine, heparin and neutral protease • Newly formed mediators include leukotrienes, prostaglandin D2 and platelet activating factor © Dr JG Lawrenson 2001 Type II Hypersensitivity © Dr JG Lawrenson 2001 • Antibody mediated hypersensitivity • Antibody directed against membrane and cell surface antigens (autoantibodies) • Antigen-antibody reactions activate complement producing membrane damage • Examples include: transfusion reactions and haemolytic disease of the newborn Type II Mechanism • Antibodies bind to cell surface • Phagocytes bind to the antibody via their Fc receptor • Phagocytosis of target cell • Antibody binding also activates complement via the classical pathway • Complement mediated cell lysis © Dr JG Lawrenson 2001 Haemolytic disease of the newborn © Dr JG Lawrenson 2001 Type III Hypersensitivity • Immune complex mediated • Excessive formation of immune complexes e.g. pesistent low-grade infection, repeated inhalation of antigens • Examples of Type III hypersensitivity include: Farmers lung, immune complex glomerulonephritis © Dr JG Lawrenson 2001 Type III Mechanism • Normally immune complexes are degraded by phagocytosis, particularly in the liver and spleen • Excessive immune complex formation results in deposition in the tissues, particularly arterioles, kidney and joints © Dr JG Lawrenson 2001 Type III Mechanism • Complexes induce platelet aggregation and complement activation • Attempted phagocytosis causes enzyme release and results in tissue damage © Dr JG Lawrenson 2001 Type IV Hypersensitivity • Delayed type hypersensitivity • Takes more than 12 hrs to develop after antigenic challenge • Examples include: contact dermatitis and tuberculin reaction • Antigens include large molecules or small molecules (haptens) linked to carrier molecules © Dr JG Lawrenson 2001 © Dr JG Lawrenson 2001 © Dr JG Lawrenson 2001 Type IV Mechanism • APC resident in the skin process antigen and migrate to regional lymph nodes where they activate T cells • Sensitised T cells migrate back to the the skin where they produce cytokines which attract macrophages which cause tissue damage © Dr JG Lawrenson 2001 © Dr JG Lawrenson 2001 © Dr JG Lawrenson 2001 Autoimmunity • Autoimmunity is a reaction of the immune system to the bodies own tissues • Self molecules are recognised as antigens due to a breakdown of self-tolerance • Antibodies (autoantibodies) react against these components • Includes organ-specific and non-organ specific diseases © Dr JG Lawrenson 2001