期刊
NATURE IMMUNOLOGY
卷 11, 期 12, 页码 1093-U97出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1952
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资金
- National Institutes of Health [R01 AI39480, R01 AI61570, R01 AI74878, F32 AI072816]
- Australian National Health and Medical Research Council
- National Cancer Institute Comprehensive Cancer Center [CA21765]
- American Lebanese Syrian Associated Charities
Regulatory T cells (T-reg cells) have a critical role in the maintenance of immunological self-tolerance. Here we show that treatment of naive human or mouse T cells with IL-35 induced a regulatory population, which we call 'iT(R)35 cells', that mediated suppression via IL-35 but not via the inhibitory cytokines IL-10 or transforming growth factor-beta (TGF-beta). We found that iT(R)35 cells did not express or require the transcription factor Foxp3, and were strongly suppressive and stable in vivo. T-reg cells induced the generation of iT(R)35 cells in an IL-35- and IL-10-dependent manner in vitro and induced their generation in vivo under inflammatory conditions in intestines infected with Trichuris muris and within the tumor microenvironment (B16 melanoma and MC38 colorectal adenocarcinoma), where they contributed to the regulatory milieu. Thus, iT(R)35 cells constitute a key mediator of infectious tolerance and contribute to T-reg cell-mediated tumor progression. Furthermore, iT(R)35 cells generated ex vivo might have therapeutic utility.
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