NK1.1- CD4+ NKG2D+ T cells suppress DSS-induced colitis in mice through production of TGF-β.
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ABSTRACT: CD4+ NKG2D+ T cells are associated with tumour, infection and autoimmune diseases. Some CD4+ NKG2D+ T cells secrete IFN-γ and TNF-α to promote inflammation, but others produce TGF-β 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-β and FasL without secreting IFN-γ, 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-β. 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-γt. Thus, NK1.1- CD4+ NKG2D+ cells exhibited immune regulatory functions, and this T cell subset could be developed to suppress inflammation in clinics.
SUBMITTER: Qian X
PROVIDER: S-EPMC5487917 | biostudies-literature |
REPOSITORIES: biostudies-literature
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