Immunological mechanisms in the reaction between drugs and the skin.
Many reactions in the skin caused by drugs would appear to be due to immunological mechanisms. Simple chemical sensitizers become antigenic after combination with carrier proteins. The bonds between the hapten and the protein are not necessarily covalent, and it is likely that weaker linkages such as hydrogen bonding or Van der Waal's forces may be involved. Reactions may be due to humoral antibody or cell-mediated immunity. Experimental models are discussed in which there is competition between B suppressor cells and T effector cells. In these situations, drugs that affect the suppressor cell system specifically can reverse a state of immunological tolerance or increase the intensity of a chemical sensitivity. Finally, the mechanism of fixed drug eruptions is discussed. It is suggested that the actions which follow the systemic absorption of the chemical and always occur at this same site are due to B cells or B cell products that remain from a previous delayed hypersensitivity reaction to the same antigen. These cells would have arrived initially as part of the non-specific inflammatory infiltrate. The initial reaction may even have been subliminal in intensity.
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D002352:Carrier Proteins / Q000378:metabolism; D003429:Cross Reactions; D003875:Drug Eruptions / Q000276:immunology*; D006168:Guinea Pigs; D006241:Haptens; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007111:Immunity, Cellular; D007114:Immunization; D010851:Picrates / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D002352:Carrier Proteins; D006241:Haptens; D010851:Picrates