期刊
NATURE IMMUNOLOGY
卷 9, 期 12, 页码 1347-1355出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1677
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资金
- US National Institutes of Health [R01AI073542-01, 1R01NS045937-01, 2R01NS35685-06, 2R37NS30843-11, 1R01A144880-03, 2P01A139671-07, 1P01NS38037-04, 1R01NS046414]
- National Multiple Sclerosis Society [RG-2571-D-9, RG-3882-A-1]
- Juvenile Diabetes Research Foundation Center for Immunological Tolerance at Harvard Medical School
- National Multiple Sclerosis Society, New York
Transcription factor Foxp3 is critical for generating regulatory T cells (T-reg cells). Transforming growth factor-beta (TGF-beta) induces Foxp3 and suppressive T-reg cells from naive T cells, whereas interleukin 6 (IL-6) inhibits the generation of inducible Treg cells. Here we show that IL-4 blocked the generation of TGF-beta-induced Foxp3(+) T-reg cells and instead induced a population of T helper cells that produced IL-9 and IL-10. The IL-9(+)IL-10(+) T cells demonstrated no regulatory properties despite producing abundant IL-10. Adoptive transfer of IL-9(+)IL-10(+) T cells into recombination-activating gene 1-deficient mice induced colitis and peripheral neuritis, the severity of which was aggravated if the IL-9(+)IL-10(+) T cells were transferred with CD45RB(hi) CD4(+) effector T cells. Thus IL-9(+)IL-10(+) T cells lack suppressive function and constitute a distinct population of helper-effector T cells that promote tissue inflammation.
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