期刊
NATURE MEDICINE
卷 6, 期 2, 页码 215-218出版社
NATURE AMERICA INC
DOI: 10.1038/72329
关键词
-
资金
- NIAID NIH HHS [R01AI32951, R01AI20922, R01AI42287] Funding Source: Medline
The development of many autoimmune diseases has been etiologically linked to exposure to infectious agents(1). For example, a subset of patients with a history of Salmonella infection develop reactive arthritis(2-6). The persistence of bacterial antigen in arthritic tissue and the isolation of Salmonella or Yersinia reactive CD8(+) T cells from the joints of patients with reactive arthritis support the etiological link between Gram-negative bacterial infection and autoimmune disease(7,8). Models proposed to account for the link between infection and autoimmunity include inflammation-induced presentation of cryptic self-epitopes, antigen persistence and molecular mimicry(1). Several studies support molecular mimicry as a mechanism for the involvement of class II epitopes in infectious disease-induced self-reactivity(9-12). Here, we have identified an immunodominant epitope derived from the S. typhimurium GroEL molecule. This epitope is presented by the mouse H2-T23-encoded class Ib molecule Qa-l and was recognized by CD8(+) cytotoxic T lymphocytes induced after natural infection. S. typhimurium-stimulated cytotoxic T lymphocytes recognizing the GroEL epitope cross-reacted with a peptide derived from mouse heat shock protein 60 and recognized stressed macrophages. Our results indicate involvement of MHC class ib molecules in infection-induced autoimmune recognition and indicate a mechanism for the etiological link between Gram-negative bacterial infection and autoimmunity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据