Helper T lymphocytes are normally only stimulated to initiate an immun
e reaction through the recognition of peptides bound to class II major
histocompatibility complex (MHC) molecules. Class II MHC molecules ar
e constitutively expressed on antigen-presenting cells which play a cr
itical role in the initiation of immune responses. In disease states,
however, other cells often express class II MHC molecules inappropriat
ely. This article suggests an hypothesis for the pathogenesis of autoi
mmune diseases based on molecular mimicry. The mimicry described is be
tween microbial or viral peptides presented by antigen-presenting cell
s and self peptides presented inappropriately on a target tissue. This
leads to helper T cells, stimulated by peptides derived from infectio
us organisms, initiating an autoimmune attack on the target tissue.