期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 4, 页码 1710-1720出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0902796
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资金
- National Institutes of Health [R01AI073542-01, 1R01NS045937-01, 2R01NS35685-06, 2R37NS30843-11, 1R01A144880-03, 2P01A139671-07, 1P01NS38037-04, 1R01NS046414, AI32412, P01 AI56296]
- National Multiple Sclerosis Society [RG-2571-D-9, RG-3882-A-1]
- Juvenile Diabetes Research Foundation Center for Immunological Tolerance at Harvard Medical School the National Institutes of Health
- Ellison Medical Foundation
- Human Frontiers Science Program
- Irvington Institute
- National Multiple Sclerosis Society
- Deutsche Forschungsgemeinschaft
IL-23 plays an important role in autoimmune tissue inflammation and induces the generation of not fully characterized effector cells that mediate protection against pathogens. In this paper, we established the essential role of IL-23R in the host response against intracellular pathogens. IL-23 was critical for the expansion or maintenance of gamma delta and double negative (DN) alpha beta T cells. These cells were rapidly recruited to the site of infection and produced large amounts of IL-17, IFN-gamma, and TNF-alpha. Notably, DN T cells transferred into L monocytogenes-infected RAG2(-/-) mice prevented bacterial growth, confirming their protective role against intracellular pathogens. Our results show that IL-23 regulates the function of IL-17-producing gamma delta and DN T cells, two essential components of the early protective immune response directed against intracellular pathogens. The Journal of Immunology, 2010, 184: 1710-1720.
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