AUTOIMMUNE-DISEASE AND MOLECULAR MIMICRY - AN HYPOTHESIS

被引:63
作者
BAUM, H
BUTLER, P
DAVIES, H
STERNBERG, MJE
BURROUGHS, AK
机构
[1] KINGS COLL,SCH LIFE BASIC MED & HLTH SCI,LONDON W8 7AH,ENGLAND
[2] IMPERIAL CANC RES FUND,BIOMOLEC MODELLING LAB,LONDON WC2A 3PX,ENGLAND
关键词
D O I
10.1016/0968-0004(93)90022-F
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:140 / 144
页数:5
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