NK1.1(-) CD4(+) NKG2D(+) T cells suppress DSS-induced colitis in mice through production of TGF-β.
NK1.1(-) CD4(+) NKG2D(+) T cells suppress DSS-induced colitis in mice through production of TGF-β.
复制标题
NK1.1â CD4 NKG2D T 细胞通过产生 TGF-β 抑制 DSS 诱导的小鼠结肠炎
DOI：
10.1111/jcmm.13072
复制
发表时间：
2017-07
影响因子：
5.3
通讯作者：
Gong W
中科院分区：
文献类型：
--
作者：
Qian X;Hu C;Han S;Lin Z;Xiao W;Ding Y;Zhang Y;Qian L;Jia X;Zhu G;Gong W
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.
