抄録
Considerable evidence has been accumulated showing that most cases of insulindependent diabetes mellitus (IDDM) are a consequence of progressive beta cell destruction during a lengthy asymptomatic period. While genetic susceptibility appears to be a prerequisite for the development of the disease, concordance for IDDM between identical twins only approaches 50%, suggesting that environmental factors must also be involved in the expression of the disease.
Several immunological abnormalities precede the onset of IDDM. Circulating islet cell autoantibodies and cell-mediated immune responses have been detected during the prediabetic period. Beta cell autoantigens, such as glutamic acid decarboxylase, 38 kD autoantigens, 52 kD autoantigens, heat shock proteins and insulin molecules have been considered to be involved in the initiation or process of beta cell-specific autoimmunity. Both CD4+ and CD8+ T cell subsets are thought to be implicated in the destruction of pancreatic beta cells. Autoreactive CD4+ T cells may be able to effect beta cell damage by non-specific inflammatory mechanisms, such as releasing beta cell cytotoxic cytokines, while CD8+ cytotoxic T cells may be involved in the destruction of pancreatic beta cells as final effectors assisted by CD4+ T cells.
