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This document summarizes hypersensitivity type III reactions, which involve tissue damage caused by antigen-antibody immune complexes depositing in tissues and activating the complement system. Small immune complexes remain in circulation and can deposit in narrow vessels of joints, kidneys, and skin, activating complement and causing increased permeability, histamine release, platelet stickiness, and inflammatory cell attraction. This leads to symptoms like swollen painful joints, skin rashes, or kidney damage depending on the deposition site. Subacute bacterial endocarditis can also result in circulating immune complexes.
Originalbeschreibung:
Mechanism of Hypersensitivity Type III and related Diseases
This document summarizes hypersensitivity type III reactions, which involve tissue damage caused by antigen-antibody immune complexes depositing in tissues and activating the complement system. Small immune complexes remain in circulation and can deposit in narrow vessels of joints, kidneys, and skin, activating complement and causing increased permeability, histamine release, platelet stickiness, and inflammatory cell attraction. This leads to symptoms like swollen painful joints, skin rashes, or kidney damage depending on the deposition site. Subacute bacterial endocarditis can also result in circulating immune complexes.
This document summarizes hypersensitivity type III reactions, which involve tissue damage caused by antigen-antibody immune complexes depositing in tissues and activating the complement system. Small immune complexes remain in circulation and can deposit in narrow vessels of joints, kidneys, and skin, activating complement and causing increased permeability, histamine release, platelet stickiness, and inflammatory cell attraction. This leads to symptoms like swollen painful joints, skin rashes, or kidney damage depending on the deposition site. Subacute bacterial endocarditis can also result in circulating immune complexes.
• Characterized by tissue damage caused by the activation of
complement in response to antigen-antibody (immune) complexes that are deposited in tissues.
• The classes of antibody involved are the same ones that
participate in type II reactions—IgG and IgM—but the mechanism by which tissue damage is brought about is different. Hypersensitivity Type III • The consequences of antigen-and-antibody interaction within the bloodstream vary according to whether the complexes formed are large, in which case they are usually trapped and removed by macrophages in the liver, spleen, and bone marrow, or small, in which case they remain in the circulation. Large Complex Small Complex • Large complexes occur when • Occurs when the ratio of antibody more than enough antibody is to antigen is enough to form only present to bind to all the antigen small complexes molecules. • It causes the complement to • They form aggregates from many activate. antigen molecules cross-linked together by the multiple binding • the complexes tend to settle in sites of IgG and IgM antibodies. the narrow capillary vessels of the synovial tissue, kidney and skin • The activation of complement leads to: – increased permeability of the blood vessels – release of histamine – stickiness of platelets – attraction of granulocytes and macrophages
• becomes more important when the antigen-antibody
complexes are deposited in blood vessels than when they are deposited in the tissues outside the capillaries. • The symptoms, depending on where the damage occurs, are swollen, painful joints, a raised skin rash, nephritis (kidney damage, causing blood proteins and even red blood cells to leak into the urine), diminished blood flow to the brain, or gut spasms.
• The formation of troublesome antigen-antibody complexes in the
blood can also result from subacute bacterial endocarditis, a chronic infection of damaged heart valves. – The infectious agent is often Streptococcus viridans, normally a harmless inhabitant of the mouth. – The bacteria in the heart become covered with a layer of fibrin, which protects them from destruction by granulocytes, while they continue to release antigens into the circulation.