期刊
IMMUNITY
卷 33, 期 5, 页码 736-751出版社
CELL PRESS
DOI: 10.1016/j.immuni.2010.10.017
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类别
资金
- Deutsche Forschungsgemeinschaft [Di764/3, GRK1104, SGBM, CRC620]
- BMBF
- Max-Planck-Society (IMPRS-MCB)
- Swiss National Science Foundation [PP00A-116894/1]
- National Institutes of Health [R37AI033068, CA069381, AI088445]
- Cluster of Excellence Inflammation at Interfaces [EXC306]
Whether the recently identified innate lymphocyte population coexpressing natural killer cell receptors (NKRs) and the nuclear receptor ROR gamma t is part of the NK or lymphoid tissue inducer (LTi) cell lineage remains unclear. By using adoptive transfer of genetically tagged LTi-like cells, we demonstrate that NKR-ROR gamma t(+) innate lymphocytes but not NK cells were direct progenitors to NKR+ROR gamma t(+) cells in vivo. Genetic lineage tracing revealed that the differentiation of LTi-like cells was characterized by the stable upregulation of NKRs and a progressive loss of ROR gamma t expression. Whereas interleukin-7 (IL-7) and intestinal microbiota stabilized ROR gamma t expression within such NKR-LTi cells, IL-12 and IL-15 accelerated ROR gamma t loss. ROR gamma t(+) NKR-LTi cells produced IL-22, whereas ROR gamma t(-) NKR-LTi cells released IFN-gamma and were potent inducers of colitis. Thus, the ROR gamma t gradient in NKR-LTi cells serves as a tunable rheostat for their functional program. Our data also define a previously unappreciated role of ROR gamma t(-) NKR-LTi cells for the onset or maintenance of inflammatory bowel diseases.
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