Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing numerous mediators that induce type I allergic reactions. These reactions primarily affect the skin, gastrointestinal tract, and respiratory systems.
Type II reactions involve IgG and IgM antibodies, which interact with host cells modified by the drug. This interaction stimulates the complement system, a part of the immune system that enhances the ability of antibodies to clear microbes and damaged cells.
Type III reactions are mediated by antibodies attached to soluble antigens, also known as immune complexes. These activate the complement system and prompt the release of mediators, resulting in inflammatory responses.
Finally, type IV hypersensitivity reactions, also known as delayed-type hypersensitivity reactions or cell-mediated hypersensitivity reactions, do not involve antibodies. Instead they are mediated by activated T-cells. These T-cells release cytokines, crucial proteins in cell signaling, which recruit macrophages and neutrophils to trigger an inflammatory response.
