Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy
Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report,...
Ausführliche Beschreibung
Autor*in: |
He, Yu-Fei [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2005 |
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Schlagwörter: |
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Anmerkung: |
© Springer-Verlag 2005 |
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Übergeordnetes Werk: |
Enthalten in: Cancer immunology immunotherapy - Berlin : Springer, 1976, 54(2005), 9 vom: 18. März, Seite 891-897 |
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Übergeordnetes Werk: |
volume:54 ; year:2005 ; number:9 ; day:18 ; month:03 ; pages:891-897 |
Links: |
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DOI / URN: |
10.1007/s00262-004-0654-1 |
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Katalog-ID: |
SPR003218538 |
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245 | 1 | 0 | |a Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
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520 | |a Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. | ||
650 | 4 | |a Interferon-γ |7 (dpeaa)DE-He213 | |
650 | 4 | |a Immune evasion |7 (dpeaa)DE-He213 | |
650 | 4 | |a Tumor development |7 (dpeaa)DE-He213 | |
650 | 4 | |a PD-L |7 (dpeaa)DE-He213 | |
650 | 4 | |a Tumor immunotherapy |7 (dpeaa)DE-He213 | |
700 | 1 | |a Wang, Xiao-Hong |4 aut | |
700 | 1 | |a Zhang, Gui-Mei |4 aut | |
700 | 1 | |a Chen, Hong-Tao |4 aut | |
700 | 1 | |a Zhang, Hui |4 aut | |
700 | 1 | |a Feng, Zuo-Hua |4 aut | |
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10.1007/s00262-004-0654-1 doi (DE-627)SPR003218538 (SPR)s00262-004-0654-1-e DE-627 ger DE-627 rakwb eng He, Yu-Fei verfasserin aut Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. Interferon-γ (dpeaa)DE-He213 Immune evasion (dpeaa)DE-He213 Tumor development (dpeaa)DE-He213 PD-L (dpeaa)DE-He213 Tumor immunotherapy (dpeaa)DE-He213 Wang, Xiao-Hong aut Zhang, Gui-Mei aut Chen, Hong-Tao aut Zhang, Hui aut Feng, Zuo-Hua aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 54(2005), 9 vom: 18. März, Seite 891-897 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:54 year:2005 number:9 day:18 month:03 pages:891-897 https://dx.doi.org/10.1007/s00262-004-0654-1 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 54 2005 9 18 03 891-897 |
spelling |
10.1007/s00262-004-0654-1 doi (DE-627)SPR003218538 (SPR)s00262-004-0654-1-e DE-627 ger DE-627 rakwb eng He, Yu-Fei verfasserin aut Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. Interferon-γ (dpeaa)DE-He213 Immune evasion (dpeaa)DE-He213 Tumor development (dpeaa)DE-He213 PD-L (dpeaa)DE-He213 Tumor immunotherapy (dpeaa)DE-He213 Wang, Xiao-Hong aut Zhang, Gui-Mei aut Chen, Hong-Tao aut Zhang, Hui aut Feng, Zuo-Hua aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 54(2005), 9 vom: 18. März, Seite 891-897 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:54 year:2005 number:9 day:18 month:03 pages:891-897 https://dx.doi.org/10.1007/s00262-004-0654-1 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 54 2005 9 18 03 891-897 |
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10.1007/s00262-004-0654-1 doi (DE-627)SPR003218538 (SPR)s00262-004-0654-1-e DE-627 ger DE-627 rakwb eng He, Yu-Fei verfasserin aut Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. Interferon-γ (dpeaa)DE-He213 Immune evasion (dpeaa)DE-He213 Tumor development (dpeaa)DE-He213 PD-L (dpeaa)DE-He213 Tumor immunotherapy (dpeaa)DE-He213 Wang, Xiao-Hong aut Zhang, Gui-Mei aut Chen, Hong-Tao aut Zhang, Hui aut Feng, Zuo-Hua aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 54(2005), 9 vom: 18. März, Seite 891-897 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:54 year:2005 number:9 day:18 month:03 pages:891-897 https://dx.doi.org/10.1007/s00262-004-0654-1 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 54 2005 9 18 03 891-897 |
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10.1007/s00262-004-0654-1 doi (DE-627)SPR003218538 (SPR)s00262-004-0654-1-e DE-627 ger DE-627 rakwb eng He, Yu-Fei verfasserin aut Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. Interferon-γ (dpeaa)DE-He213 Immune evasion (dpeaa)DE-He213 Tumor development (dpeaa)DE-He213 PD-L (dpeaa)DE-He213 Tumor immunotherapy (dpeaa)DE-He213 Wang, Xiao-Hong aut Zhang, Gui-Mei aut Chen, Hong-Tao aut Zhang, Hui aut Feng, Zuo-Hua aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 54(2005), 9 vom: 18. März, Seite 891-897 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:54 year:2005 number:9 day:18 month:03 pages:891-897 https://dx.doi.org/10.1007/s00262-004-0654-1 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 54 2005 9 18 03 891-897 |
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10.1007/s00262-004-0654-1 doi (DE-627)SPR003218538 (SPR)s00262-004-0654-1-e DE-627 ger DE-627 rakwb eng He, Yu-Fei verfasserin aut Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2005 Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. Interferon-γ (dpeaa)DE-He213 Immune evasion (dpeaa)DE-He213 Tumor development (dpeaa)DE-He213 PD-L (dpeaa)DE-He213 Tumor immunotherapy (dpeaa)DE-He213 Wang, Xiao-Hong aut Zhang, Gui-Mei aut Chen, Hong-Tao aut Zhang, Hui aut Feng, Zuo-Hua aut Enthalten in Cancer immunology immunotherapy Berlin : Springer, 1976 54(2005), 9 vom: 18. März, Seite 891-897 (DE-627)253390443 (DE-600)1458489-X 1432-0851 nnns volume:54 year:2005 number:9 day:18 month:03 pages:891-897 https://dx.doi.org/10.1007/s00262-004-0654-1 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 54 2005 9 18 03 891-897 |
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Enthalten in Cancer immunology immunotherapy 54(2005), 9 vom: 18. März, Seite 891-897 volume:54 year:2005 number:9 day:18 month:03 pages:891-897 |
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Enthalten in Cancer immunology immunotherapy 54(2005), 9 vom: 18. März, Seite 891-897 volume:54 year:2005 number:9 day:18 month:03 pages:891-897 |
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Cancer immunology immunotherapy |
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He, Yu-Fei @@aut@@ Wang, Xiao-Hong @@aut@@ Zhang, Gui-Mei @@aut@@ Chen, Hong-Tao @@aut@@ Zhang, Hui @@aut@@ Feng, Zuo-Hua @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR003218538</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519230553.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201001s2005 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00262-004-0654-1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR003218538</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00262-004-0654-1-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">He, Yu-Fei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2005</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Springer-Verlag 2005</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. 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author |
He, Yu-Fei |
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He, Yu-Fei misc Interferon-γ misc Immune evasion misc Tumor development misc PD-L misc Tumor immunotherapy Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
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Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy Interferon-γ (dpeaa)DE-He213 Immune evasion (dpeaa)DE-He213 Tumor development (dpeaa)DE-He213 PD-L (dpeaa)DE-He213 Tumor immunotherapy (dpeaa)DE-He213 |
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Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
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Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
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sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
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Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
abstract |
Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. © Springer-Verlag 2005 |
abstractGer |
Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. © Springer-Verlag 2005 |
abstract_unstemmed |
Abstract Although the proinflammatory cytokine interferon-γ (IFN-γ) has been generally thought to enhance antitumor immune responses and be involved in antitumor mechanisms of many other immunotherapy molecules, it has also been reported that IFN-γ could promote tumor immune evasion. In this report, by using an ideal mouse model that expresses IFN-γ locally in muscle, we demonstrate that sustained low-level expression of IFN-γ promotes the development of several types of tumor including H22 hepatoma, MA782/5S mammary adenocarcinoma and B16 melanoma. However, transitory expression of IFN-γ does not have such an effect. On the other hand, sustained high-level expression of IFN-γ mediates significant antitumor effect on H22 hepatoma. Low level of IFN-γ upregulates expression of PD-L1, PD-L2, CTLA-4 and Foxp3, which may partly account for the tumor immune evasion promoted by IFN-γ. Furthermore, blockade of PD-L inhibits IFN-γ’s tumor-promoting effect. Our findings provide a mechanistic link between chronic inflammation and cancer and would have potential implications for cancer prevention and also for the design of cytokine–based cancer immunotherapy. © Springer-Verlag 2005 |
collection_details |
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container_issue |
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title_short |
Sustained low-level expression of interferon-γ promotes tumor development: potential insights in tumor prevention and tumor immunotherapy |
url |
https://dx.doi.org/10.1007/s00262-004-0654-1 |
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author2 |
Wang, Xiao-Hong Zhang, Gui-Mei Chen, Hong-Tao Zhang, Hui Feng, Zuo-Hua |
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Wang, Xiao-Hong Zhang, Gui-Mei Chen, Hong-Tao Zhang, Hui Feng, Zuo-Hua |
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doi_str |
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up_date |
2024-07-03T18:04:12.654Z |
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score |
7.4010477 |