Type III hypersensitivity, also referred to as immune complex hypersensitivity, is an excessive immune response resulting from the formation and deposition of immune complexes within various tissues and organs. This immune reaction occurs when antigens combine with antibodies to form complexes in the bloodstream. These complexes can then settle and accumulate in different organs, leading to the activation of inflammatory responses and subsequent tissue damage.
This type of hypersensitivity involves the interaction between IgG or IgM antibodies and antigens that are typically soluble or circulating immune complexes. Upon deposition, the immune complexes trigger the activation of complement proteins that initiate the inflammatory response. In addition, immune cells, such as neutrophils and macrophages, are also attracted to the site of deposition and release pro-inflammatory molecules and enzymes, causing local tissue injury.
The resulting clinical manifestations of type III hypersensitivity include a wide range of autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and vasculitis. Symptoms typically involve inflammation of multiple organs or tissues, such as joints, kidneys, and blood vessels. Examples of complications associated with type III hypersensitivity include nephritis, arthritis, and vasculitis.
Treatment approaches for type III hypersensitivity focus on managing the underlying autoimmune disease and controlling the inflammatory response. This may involve the use of immunosuppressive drugs, anti-inflammatory medications, and, in severe cases, plasma exchange to remove circulating immune complexes from the blood.
