期刊
NATURE IMMUNOLOGY
卷 17, 期 9, 页码 1084-1092出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3512
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资金
- National Institute of Diabetes and Digestive and Kidney Diseases [DK072201]
- National Institute of Allergy and Infectious Diseases [AI073899, AI080959, AI095245]
- Arthritis Foundation
- Crohn's and Colitis Foundation of America
- Burroughs Wellcome Fund
- Irma Hirschl and Monique Weill-Caulier Charitable Trust Funds
- American Cancer Society
- Leukemia and Lymphoma Society
Microbial infections often precede the onset of autoimmunity. How infections trigger autoimmunity remains poorly understood. We investigated the possibility that infection might create conditions that allow the stimulatory presentation of self peptides themselves and that this might suffice to elicit autoreactive T cell responses that lead to autoimmunity. Self-reactive CD4(+) T cells are major drivers of autoimmune disease, but their activation is normally prevented through regulatory mechanisms that limit the immunostimulatory presentation of self antigens. Here we found that the apoptosis of infected host cells enabled the presentation of self antigens by major histocompatibility complex class II molecules in an inflammatory context. This was sufficient for the generation of an autoreactive T(H)17 subset of helper T cells, prominently associated with autoimmune disease. Once induced, the self-reactive T(H)17 cells promoted auto-inflammation and autoantibody generation. Our findings have implications for how infections precipitate autoimmunity.
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