期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 102, 期 48, 页码 17418-17423出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0507454102
关键词
experimental autoimmune encephalomyelitis (EAE); multiple sclerosis; regulation; tolerance
资金
- Medical Research Council [G117/515] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- MRC [G117/515] Funding Source: UKRI
- Medical Research Council [G117/515] Funding Source: researchfish
The molecular-mimicry theory proposes that immune cross-reactivity between microbial and self-antigen is the initiating event in the activation of autoaggressive immune responses leading to autoimmune disease. In support of this possibility, it is now accepted that T cell recognition of antigen is highly degenerate. However, it is to be expected that the immune system would have evolved mechanisms to counter such a potential danger. We studied the influence of CD4(+)CD25(+) regulatory T cells (Treg) on the ability of suboptimal T cell receptor ligands to provoke autoimmunity. By using CD4(+) T cell-driven experimental autoimmune encephalomyelitis as a model, it was found that depletion of CD4(+)CD25(+)Foxp3(+) Treg allowed pathology to develop in response to suboptimal T cell stimulation. These data demonstrate the importance of Treg in raising the threshold of triggering of autoreactive T cell responses, thus limiting the risk of autoimmune disease due to molecular mimicry.
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