Type IV Autoimmune Reactions
Type IV hypersensitivity reactions are mediated by T cells that recognize peptides presented on the surface of antigen presenting cells in the context of class II major histocompatibility complex (MHC) molecules and that produce the cytokines interferon γ (IFN-γ), interleukin 3 (IL-3), tumor necrosis factor (TNF)α, TNF-β, and granulocyte-macrophage colony stimulating factor (GM-CSF). These cells constitute a subset of helper T cells termed TH1 cells. Elaboration of “TH1 cytokines” leads to macrophage recruitment and activation, enhanced expression of adhesion molecules, and increased production of monocytes by the bone marrow. Delayed type hypersensitivity in response to the intradermal injection of certain antigens, such as tuberculin (used for tuberculosis skin testing), is a classic example of a type IV hypersensitivity reaction. In the case of autoimmunity, self-antigens (instead of foreign antigens) plus MHC molecules are recognized by the antigen receptors of TH1 cells.