Abstract
An immune response in the form of antibody production against a foreign substance is often mounted to remove any detrimental antigen from the host. In type III hypersensitivity, overproduction of immunoglobulin G (IgG) and IgM to a foreign or self‐antigen can lead to the formation and deposition of excessive amounts of insoluble intermediate‐sized immune complexes, which can be difficult to remove from various tissues by phagocytosis. This in turn may trigger classical complement activation, leading to overproduction of other inflammatory mediators, leading to the recruitment, activation and degranulation of peripheral blood granulocytes, such as basophils or an influx of marginating neutrophils to specific tissues, such as the kidneys, lungs and joints culminating in damage. Depending on the frequency of exposure and route of entry, type III hypersensitivity reactions can develop over hours, weeks or years. Examples of type III hypersensitivity reactions include drug‐induced serum sickness, farmer's lung and systemic lupus erythematosus.
Key Concepts:
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Hypersensitivity type III reactions involve the interaction of IgG or IgM immunoglobulins with antigen to form immune complexes.
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Intermediate‐sized immune complexes are difficult to remove by the process of phagocytosis.
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Complement proteins bind to immune complexes as part of the normal physiological process.
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During hypersensitivity type III reactions sustained complement–immune complex interaction leads to the production of activated complement components, responsible for the recruitment of phagocytes.
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Cell‐mediated tissue damage occurs as part of type III hypersensitivity, involving activated basophils in the peripheral circulation and marginating neutrophils in the vascular and other tissues.
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Fc receptors on the surface of granulocytes are important in inducing the immunecomplex‐mediated inflammation.
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Type III hypersensitivity reactions can manifest as acute or chronic reactions and can occur systemically or in specific tissues.
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Self and foreign antigens can provoke type III hypersensitivity reactions.
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Nonspecific immunosuppressive treatments are commonly used to treat type III hypersensitivity reactions.
Keywords: complement; granulocytes; immune complexes; Arthus reaction; vasculitis; phagocytes; immunoglobulin; rheumatoid factor; autoimmune