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NK1.1- CD4+ NKG2D+ T cells suppress DSS-induced colitis in mice through production of TGF-?.

ABSTRACT: CD4+ NKG2D+ T cells are associated with tumour, infection and autoimmune diseases. Some CD4+ NKG2D+ T cells secrete IFN-? and TNF-? to promote inflammation, but others produce TGF-? and FasL to facilitate tumour evasion. Here, murine CD4+ NKG2D+ T cells were further classified into NK1.1- CD4+ NKG2D+ and NK1.1+ CD4+ NKG2D+ subpopulations. The frequency of NK1.1- CD4+ NKG2D+ cells decreased in inflamed colons, whereas more NK1.1+ CD4+ NKG2D+ cells infiltrated into colons of mice with DSS-induced colitis. NK1.1- CD4+ NKG2D+ cells expressed TGF-? and FasL without secreting IFN-?, IL-21 and IL-17 and displayed no cytotoxicity. The adoptive transfer of NK1.1- CD4+ NKG2D+ cells suppressed DSS-induced colitis largely dependent on TGF-?. NK1.1- CD4+ NKG2D+ cells did not expressed Foxp3, CD223 (LAG-3) and GITR. The subpopulation was distinct from NK1.1+ CD4+ NKG2D+ cells in terms of surface markers and RNA transcription. NK1.1- CD4+ NKG2D+ cells also differed from Th2 or Th17 cells because the former did not express GATA-3 and ROR-?t. Thus, NK1.1- CD4+ NKG2D+ cells exhibited immune regulatory functions, and this T cell subset could be developed to suppress inflammation in clinics.


PROVIDER: S-EPMC5487917 | BioStudies | 2017-01-01T00:00:00Z

REPOSITORIES: biostudies

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