Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice
Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+}...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Lin, Zhijie [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer-Verlag GmbH Germany, part of Springer Nature 2018 |
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| Übergeordnetes Werk: |
Enthalten in: Cancer immunology immunotherapy - Berlin : Springer, 1976, 67(2018), 7 vom: 25. Mai, Seite 1159-1173 |
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| Übergeordnetes Werk: |
volume:67 ; year:2018 ; number:7 ; day:25 ; month:05 ; pages:1159-1173 |
| Links: |
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| DOI / URN: |
10.1007/s00262-018-2172-6 |
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| Katalog-ID: |
SPR003240894 |
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| 041 | |a eng | ||
| 100 | 1 | |a Lin, Zhijie |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice |
| 264 | 1 | |c 2018 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a © Springer-Verlag GmbH Germany, part of Springer Nature 2018 | ||
| 520 | |a Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. | ||
| 650 | 4 | |a Regulatory T cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a CD4 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NKG2D |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Tumor immunity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a TGF-β |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NK1.1 |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Han, Sen |4 aut | |
| 700 | 1 | |a Qian, Xingxing |4 aut | |
| 700 | 1 | |a Hu, Chunxia |4 aut | |
| 700 | 1 | |a Xiao, Weiming |4 aut | |
| 700 | 1 | |a Qian, Li |4 aut | |
| 700 | 1 | |a Zhang, Yu |4 aut | |
| 700 | 1 | |a Ding, Yanbing |4 aut | |
| 700 | 1 | |a Jia, Xiaoqin |4 aut | |
| 700 | 1 | |a Zhu, Guoqiang |4 aut | |
| 700 | 1 | |a Gong, Weijuan |0 (orcid)0000-0002-8543-1314 |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Cancer immunology immunotherapy |d Berlin : Springer, 1976 |g 67(2018), 7 vom: 25. Mai, Seite 1159-1173 |w (DE-627)253390443 |w (DE-600)1458489-X |x 1432-0851 |7 nnns |
| 773 | 1 | 8 | |g volume:67 |g year:2018 |g number:7 |g day:25 |g month:05 |g pages:1159-1173 |
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| 912 | |a GBV_ILN_2088 | ||
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| 912 | |a GBV_ILN_2107 | ||
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| 912 | |a GBV_ILN_2110 | ||
| 912 | |a GBV_ILN_2111 | ||
| 912 | |a GBV_ILN_2112 | ||
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| 912 | |a GBV_ILN_2116 | ||
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10.1007/s00262-018-2172-6 doi (DE-627)SPR003240894 (SPR)s00262-018-2172-6-e DE-627 ger DE-627 rakwb eng Lin, Zhijie verfasserin aut Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. Regulatory T cell (dpeaa)DE-He213 CD4 (dpeaa)DE-He213 NKG2D (dpeaa)DE-He213 Tumor immunity (dpeaa)DE-He213 TGF-β (dpeaa)DE-He213 NK1.1 (dpeaa)DE-He213 Han, Sen aut Qian, Xingxing aut Hu, Chunxia aut Xiao, Weiming aut Qian, Li aut Zhang, Yu aut Ding, Yanbing aut Jia, Xiaoqin aut Zhu, Guoqiang aut Gong, Weijuan (orcid)0000-0002-8543-1314 aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 67(2018), 7 vom: 25. Mai, Seite 1159-1173 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 https://dx.doi.org/10.1007/s00262-018-2172-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 67 2018 7 25 05 1159-1173 |
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10.1007/s00262-018-2172-6 doi (DE-627)SPR003240894 (SPR)s00262-018-2172-6-e DE-627 ger DE-627 rakwb eng Lin, Zhijie verfasserin aut Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. Regulatory T cell (dpeaa)DE-He213 CD4 (dpeaa)DE-He213 NKG2D (dpeaa)DE-He213 Tumor immunity (dpeaa)DE-He213 TGF-β (dpeaa)DE-He213 NK1.1 (dpeaa)DE-He213 Han, Sen aut Qian, Xingxing aut Hu, Chunxia aut Xiao, Weiming aut Qian, Li aut Zhang, Yu aut Ding, Yanbing aut Jia, Xiaoqin aut Zhu, Guoqiang aut Gong, Weijuan (orcid)0000-0002-8543-1314 aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 67(2018), 7 vom: 25. Mai, Seite 1159-1173 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 https://dx.doi.org/10.1007/s00262-018-2172-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 67 2018 7 25 05 1159-1173 |
| allfields_unstemmed |
10.1007/s00262-018-2172-6 doi (DE-627)SPR003240894 (SPR)s00262-018-2172-6-e DE-627 ger DE-627 rakwb eng Lin, Zhijie verfasserin aut Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. Regulatory T cell (dpeaa)DE-He213 CD4 (dpeaa)DE-He213 NKG2D (dpeaa)DE-He213 Tumor immunity (dpeaa)DE-He213 TGF-β (dpeaa)DE-He213 NK1.1 (dpeaa)DE-He213 Han, Sen aut Qian, Xingxing aut Hu, Chunxia aut Xiao, Weiming aut Qian, Li aut Zhang, Yu aut Ding, Yanbing aut Jia, Xiaoqin aut Zhu, Guoqiang aut Gong, Weijuan (orcid)0000-0002-8543-1314 aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 67(2018), 7 vom: 25. Mai, Seite 1159-1173 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 https://dx.doi.org/10.1007/s00262-018-2172-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 67 2018 7 25 05 1159-1173 |
| allfieldsGer |
10.1007/s00262-018-2172-6 doi (DE-627)SPR003240894 (SPR)s00262-018-2172-6-e DE-627 ger DE-627 rakwb eng Lin, Zhijie verfasserin aut Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. Regulatory T cell (dpeaa)DE-He213 CD4 (dpeaa)DE-He213 NKG2D (dpeaa)DE-He213 Tumor immunity (dpeaa)DE-He213 TGF-β (dpeaa)DE-He213 NK1.1 (dpeaa)DE-He213 Han, Sen aut Qian, Xingxing aut Hu, Chunxia aut Xiao, Weiming aut Qian, Li aut Zhang, Yu aut Ding, Yanbing aut Jia, Xiaoqin aut Zhu, Guoqiang aut Gong, Weijuan (orcid)0000-0002-8543-1314 aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 67(2018), 7 vom: 25. Mai, Seite 1159-1173 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 https://dx.doi.org/10.1007/s00262-018-2172-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 67 2018 7 25 05 1159-1173 |
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10.1007/s00262-018-2172-6 doi (DE-627)SPR003240894 (SPR)s00262-018-2172-6-e DE-627 ger DE-627 rakwb eng Lin, Zhijie verfasserin aut Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. Regulatory T cell (dpeaa)DE-He213 CD4 (dpeaa)DE-He213 NKG2D (dpeaa)DE-He213 Tumor immunity (dpeaa)DE-He213 TGF-β (dpeaa)DE-He213 NK1.1 (dpeaa)DE-He213 Han, Sen aut Qian, Xingxing aut Hu, Chunxia aut Xiao, Weiming aut Qian, Li aut Zhang, Yu aut Ding, Yanbing aut Jia, Xiaoqin aut Zhu, Guoqiang aut Gong, Weijuan (orcid)0000-0002-8543-1314 aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 67(2018), 7 vom: 25. Mai, Seite 1159-1173 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 https://dx.doi.org/10.1007/s00262-018-2172-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 67 2018 7 25 05 1159-1173 |
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Enthalten in Cancer immunology immunotherapy 67(2018), 7 vom: 25. Mai, Seite 1159-1173 volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 |
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Enthalten in Cancer immunology immunotherapy 67(2018), 7 vom: 25. Mai, Seite 1159-1173 volume:67 year:2018 number:7 day:25 month:05 pages:1159-1173 |
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Lin, Zhijie @@aut@@ Han, Sen @@aut@@ Qian, Xingxing @@aut@@ Hu, Chunxia @@aut@@ Xiao, Weiming @@aut@@ Qian, Li @@aut@@ Zhang, Yu @@aut@@ Ding, Yanbing @@aut@@ Jia, Xiaoqin @@aut@@ Zhu, Guoqiang @@aut@@ Gong, Weijuan @@aut@@ |
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|
| author |
Lin, Zhijie |
| spellingShingle |
Lin, Zhijie misc Regulatory T cell misc CD4 misc NKG2D misc Tumor immunity misc TGF-β misc NK1.1 Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice |
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Lin, Zhijie |
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springer |
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Not Illustrated |
| issn |
1432-0851 |
| topic_title |
Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice Regulatory T cell (dpeaa)DE-He213 CD4 (dpeaa)DE-He213 NKG2D (dpeaa)DE-He213 Tumor immunity (dpeaa)DE-He213 TGF-β (dpeaa)DE-He213 NK1.1 (dpeaa)DE-He213 |
| topic |
misc Regulatory T cell misc CD4 misc NKG2D misc Tumor immunity misc TGF-β misc NK1.1 |
| topic_unstemmed |
misc Regulatory T cell misc CD4 misc NKG2D misc Tumor immunity misc TGF-β misc NK1.1 |
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misc Regulatory T cell misc CD4 misc NKG2D misc Tumor immunity misc TGF-β misc NK1.1 |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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Cancer immunology immunotherapy |
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Cancer immunology immunotherapy |
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| title |
Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice |
| ctrlnum |
(DE-627)SPR003240894 (SPR)s00262-018-2172-6-e |
| title_full |
Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice |
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Lin, Zhijie |
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Cancer immunology immunotherapy |
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Cancer immunology immunotherapy |
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2018 |
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Lin, Zhijie Han, Sen Qian, Xingxing Hu, Chunxia Xiao, Weiming Qian, Li Zhang, Yu Ding, Yanbing Jia, Xiaoqin Zhu, Guoqiang Gong, Weijuan |
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Elektronische Aufsätze |
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Lin, Zhijie |
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10.1007/s00262-018-2172-6 |
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| title_sort |
regulatory nk1.$ 1^{−} %$ cd4^{+} %$ nkg2d^{+} $ subset induced by $ nkg2dl^{+} $ cells promotes tumor evasion in mice |
| title_auth |
Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice |
| abstract |
Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. © Springer-Verlag GmbH Germany, part of Springer Nature 2018 |
| abstractGer |
Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. © Springer-Verlag GmbH Germany, part of Springer Nature 2018 |
| abstract_unstemmed |
Abstract Regulatory T cells play critical roles in self-tolerance and tumor evasion. $ CD4^{+} %$ NKG2D^{+} $ cells with regulatory activity are present in patients with $ NKG2DL^{+} $ tumors and juvenile systemic lupus erythematosus. We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. Furthermore, regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells did not express Foxp3 or CD25 and expressed intermediate levels of T-bet. Western-blotting showed that STAT3 signaling was activated in NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells of MC38 tumor-bearing and pCD86-Rae-1ε transgenic mice. In conclusion, we describe a regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T-cell population, different from other regulatory T cells and abnormally elevated in pCD86-Rae-1ε transgenic and MC38 tumor-bearing mice. © Springer-Verlag GmbH Germany, part of Springer Nature 2018 |
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Regulatory NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ subset induced by $ NKG2DL^{+} $ cells promotes tumor evasion in mice |
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https://dx.doi.org/10.1007/s00262-018-2172-6 |
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Han, Sen Qian, Xingxing Hu, Chunxia Xiao, Weiming Qian, Li Zhang, Yu Ding, Yanbing Jia, Xiaoqin Zhu, Guoqiang Gong, Weijuan |
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Han, Sen Qian, Xingxing Hu, Chunxia Xiao, Weiming Qian, Li Zhang, Yu Ding, Yanbing Jia, Xiaoqin Zhu, Guoqiang Gong, Weijuan |
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10.1007/s00262-018-2172-6 |
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2024-07-03T18:14:33.019Z |
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We previously showed that TGF-β-producing $ CD4^{+} %$ NKG2D^{+} $ T cells are present in pCD86-Rae-1ε transgenic mice. Here, we performed both ex vivo and in vivo studies on pCD86-Rae-1ε transgenic mice and an MC38 tumor-bearing mouse model and show that NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells have regulatory activity in pCD86-Rae-1ε transgenic mice. Furthermore, this T-cell subset was induced in mice transplanted with $ NKG2DL^{+} $ tumor cells and produced TGF-β and FasL, and secreted low amounts of IFN-γ. This T-cell subset downregulated the function of effector T cells and dendritic cells, which were abolished by anti-TGF-β antibody. In vivo, adoptive transfer of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells promoted TGF-β-dependent tumor growth in mice. We further found that ex vivo induction of NK1.$ 1^{−} %$ CD4^{+} %$ NKG2D^{+} $ T cells was dependent on both anti-CD3 and NKG2DL stimulation. 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| score |
7.3999224 |