NK1.1− CD4+ NKG2D+ T cells suppress DSS‐induced colitis in mice through production of TGF‐β. Issue 7 (22nd February 2017)

• Record Type: Journal Article
• Authors: Qian, Xingxing; Hu, Chunxia; Han, Sen; Lin, Zhijie; Xiao, Weiming; Ding, Yanbing; Zhang, Yu; Qian, Li; Jia, Xiaoqing; Zhu, Guoqiang; Gong, Weijuan
• Is Part Of: Journal of cellular and molecular medicine. Volume 21:Issue 7(2017)
• Page Start: 1431
• Page End: 1444
• Publication Date: 2017-02-22
• Subjects: CD4 -- NKG2D -- colitis -- NK1.1 -- regulatory; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.13072
• Languages: English
• ISSNs: 1582-1838

Abstract

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.