UCL logo

UCL Discovery

UCL home » Library Services » Electronic resources » UCL Discovery

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.

Full text not available from this repository.

Abstract

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.

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

Archive Staff Only: edit this record