Autoimmune mechanisms in the pathogenesis of rheumatic fever.
The etiologic agent of acute rheumatic fever is the group A streptococcus; however, its role in the pathogenesis of this disease is not well understood. Epidemiologic and immunologic evidence suggests that there is a population at risk and that the nature of the host response to streptococcal antigens and the physicochemical nature of the streptococcal antigens all play a significant role in determining the natural history of the disease process. Furthermore, the genetic control of the interaction of the host with the streptococci is clearly involved in a set of events--as yet obscure--that result in acute rheumatic fever. Neither antibody-mediated nor cell-mediated hypersensitivity reactions have been demonstrated in vivo or in vitro that wholly reproduce the characteristics of this disease. Additional studies of the regulation of the immune response and of human immunogenetics are essential for gaining further insight into the pathogenesis of acute rheumatic fever.