Molecular mimicry and the pathogenesis of insulin-dependent diabetes mellitus: still just an attractive hypothesis

An abundant body of literature suggests that the cellular immune system plays a key role in the autoimmune destruction of insulin-secreting pancreatic beta cells that results in insulin-dependent diabetes mellitus (IDDM). For years, studies have supported the concept that molecular mimicry, a process of antigenic crossreactivity resulting from similarity in amino acid sequence or structure, could be one pathway whereby this disease is induced or its natural history modulated. However, the transfer of this 'hypothesis' to that of a proven mechanism underlying this clinical disorder has been slow and never fully achieved. This article reviews the theoretical basis for molecular mimicry in autoimmune disease and the evidence supporting its role in the pathogenesis of IDDM.