title: NK1.1-CD4+NKG2D+T cells suppress DSS-induced colitis in mice through production of TGF-β.
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.
authors.affiliation: Department of Immunology, School of Medicine, Yangzhou University, Yangzhou, China.
authors.forename: Xingxing
authors.initials: X
authors.lastname: Qian
authors.affiliation: Department of Immunology, School of Medicine, Yangzhou University, Yangzhou, China.
authors.forename: Chunxia
authors.initials: C
authors.lastname: Hu
authors.affiliation: Department of Immunology, School of Medicine, Yangzhou University, Yangzhou, China.
authors.forename: Sen
authors.initials: S
authors.lastname: Han
authors.affiliation: Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, China.|Jiangsu Key Laboratory of Zoonosis, Yangzhou, China.
authors.forename: Zhijie
authors.initials: Z
authors.lastname: Lin
authors.affiliation: Department of Gastroenterology, The Second Clinical Medical College, Yangzhou University, Yangzhou, China.
authors.forename: Weiming
authors.initials: W
authors.lastname: Xiao
authors.affiliation: Department of Gastroenterology, The Second Clinical Medical College, Yangzhou University, Yangzhou, China.
authors.forename: Yanbing
authors.initials: Y
authors.lastname: Ding
authors.affiliation: Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Immunology, School of Medicine, Yangzhou University, Yangzhou, China.
authors.forename: Li
authors.initials: L
authors.lastname: Qian
authors.affiliation: Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, China.
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Jia
authors.affiliation: Jiangsu Key Laboratory of Zoonosis, Yangzhou, China.|Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China.
authors.forename: Guoqiang
authors.initials: G
authors.lastname: Zhu
authors.affiliation: Department of Immunology, School of Medicine, Yangzhou University, Yangzhou, China.|Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, China.|Jiangsu Key Laboratory of Zoonosis, Yangzhou, China.|Department of Gastroenterology, The Second Clinical Medical College, Yangzhou University, Yangzhou, China.|Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China.
authors.forename: Weijuan
authors.initials: W
authors.lastname: Gong
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000235:genetics* / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D019070:Cell Lineage / Q000235:genetics / Q000276:immunology; D003092:Colitis / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D016264:Dextran Sulfate / Q000633:toxicity; D053222:Fas Ligand Protein / Q000235:genetics; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D020381:Interleukin-17 / Q000235:genetics; D007378:Interleukins / Q000235:genetics; D051379:Mice; D055651:NK Cell Lectin-Like Receptor Subfamily B / Q000235:genetics* / Q000276:immunology; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000235:genetics* / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000235:genetics* / Q000276:immunology; D000098546:Interleukin-21
chemical_list: D000950:Antigens, Ly; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D020381:Interleukin-17; D007378:Interleukins; C527211:Klrb1c protein, mouse; C527086:Klrk1 protein, mouse; D055651:NK Cell Lectin-Like Receptor Subfamily B; D055655:NK Cell Lectin-Like Receptor Subfamily K; D016212:Transforming Growth Factor beta; D007371:Interferon-gamma; D016264:Dextran Sulfate; D000098546:Interleukin-21
keywords: CD4; NK1.1; NKG2D; colitis; regulatory