期刊
NATURE IMMUNOLOGY
卷 10, 期 11, 页码 1178-U61出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1791
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资金
- US National Institutes of Health [PO1 DK46763, RO1 AI057992, RO1 AI50265]
- Crohn's & Colitis Foundation of America
Regulatory T cells (T-reg cells) that express the transcription factor Foxp3 suppress the activity of other cells. Here we show that interleukin 10 (IL-10) produced by CD11b(+) myeloid cells in recombination-activating gene 1-deficient (Rag1(-/-)) recipient mice was needed to prevent the colitis induced by transferred CD4(+)CD45RB(hi) T cells. In Il10(-/-)Rag1(-/-) mice, T-reg cells failed to maintain Foxp3 expression and regulatory activity. The loss of Foxp3 expression occurred only in recipients with colitis, which indicates that the requirement for IL-10 is manifested in the presence of inflammation. IL-10 receptor-deficient (Il10rb(-/-)) T-reg cells also failed to maintain Foxp3 expression, which suggested that host IL-10 acted directly on the T-reg cells. Our data indicate that IL-10 released from myeloid cells acts in a paracrine manner on T-reg cells to maintain Foxp3 expression.
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