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NK1.1(−) CD4(+) NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β
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...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5487917/ https://www.ncbi.nlm.nih.gov/pubmed/28224733 http://dx.doi.org/10.1111/jcmm.13072 |
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author | Qian, Xingxing Hu, Chunxia Han, Sen Lin, Zhijie Xiao, Weiming Ding, Yanbing Zhang, Yu Qian, Li Jia, Xiaoqing Zhu, Guoqiang Gong, Weijuan |
author_facet | Qian, Xingxing Hu, Chunxia Han, Sen Lin, Zhijie Xiao, Weiming Ding, Yanbing Zhang, Yu Qian, Li Jia, Xiaoqing Zhu, Guoqiang Gong, Weijuan |
author_sort | Qian, Xingxing |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5487917 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54879172017-07-04 NK1.1(−) CD4(+) NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β Qian, Xingxing Hu, Chunxia Han, Sen Lin, Zhijie Xiao, Weiming Ding, Yanbing Zhang, Yu Qian, Li Jia, Xiaoqing Zhu, Guoqiang Gong, Weijuan J Cell Mol Med Original Articles 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. John Wiley and Sons Inc. 2017-02-22 2017-07 /pmc/articles/PMC5487917/ /pubmed/28224733 http://dx.doi.org/10.1111/jcmm.13072 Text en © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Qian, Xingxing Hu, Chunxia Han, Sen Lin, Zhijie Xiao, Weiming Ding, Yanbing Zhang, Yu Qian, Li Jia, Xiaoqing Zhu, Guoqiang Gong, Weijuan NK1.1(−) CD4(+) NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β |
title |
NK1.1(−)
CD4(+)
NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β |
title_full |
NK1.1(−)
CD4(+)
NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β |
title_fullStr |
NK1.1(−)
CD4(+)
NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β |
title_full_unstemmed |
NK1.1(−)
CD4(+)
NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β |
title_short |
NK1.1(−)
CD4(+)
NKG2D(+) T cells suppress DSS‐induced colitis in mice through production of TGF‐β |
title_sort | nk1.1(−)
cd4(+)
nkg2d(+) t cells suppress dss‐induced colitis in mice through production of tgf‐β |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5487917/ https://www.ncbi.nlm.nih.gov/pubmed/28224733 http://dx.doi.org/10.1111/jcmm.13072 |
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