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Autoimmune disease and molecular mimicry: an hypothesis.

Baum, H; Butler, P; Davies, H; Sternberg, MJ; Burroughs, AK; (1993) Autoimmune disease and molecular mimicry: an hypothesis. Trends Biochem Sci , 18 (4) 140 - 144.

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

Title:Autoimmune disease and molecular mimicry: an hypothesis.
Keywords:Amino Acid Sequence, Autoantigens, Autoimmune Diseases, Female, Histocompatibility Antigens Class II, Humans, Models, Biological, Molecular Sequence Data

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