IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation
Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis...
Ausführliche Beschreibung
Autor*in: |
Mudter, Jonas [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2009 |
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Schlagwörter: |
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Anmerkung: |
© L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 |
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Übergeordnetes Werk: |
Enthalten in: Archivum immunologiae et therapiae experimentalis - [Cham (ZG)] : [Springer International Publishing AG], 1994, 57(2009), 5 vom: 20. Aug., Seite 369-376 |
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Übergeordnetes Werk: |
volume:57 ; year:2009 ; number:5 ; day:20 ; month:08 ; pages:369-376 |
Links: |
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DOI / URN: |
10.1007/s00005-009-0046-5 |
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Katalog-ID: |
SPR000040010 |
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520 | |a Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. | ||
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650 | 4 | |a IL-17 |7 (dpeaa)DE-He213 | |
700 | 1 | |a Yu, Jingling |4 aut | |
700 | 1 | |a Amoussina, Lioubov |4 aut | |
700 | 1 | |a Weigmann, Benno |4 aut | |
700 | 1 | |a Hoffman, Arthur |4 aut | |
700 | 1 | |a Rücknagel, Katrin |4 aut | |
700 | 1 | |a Galle, Peter R. |4 aut | |
700 | 1 | |a Neurath, Markus F. |4 aut | |
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10.1007/s00005-009-0046-5 doi (DE-627)SPR000040010 (SPR)s00005-009-0046-5-e DE-627 ger DE-627 rakwb eng Mudter, Jonas verfasserin aut IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. IRF4 (dpeaa)DE-He213 T cells (dpeaa)DE-He213 interferon regulatory factor (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 IL-17 (dpeaa)DE-He213 Yu, Jingling aut Amoussina, Lioubov aut Weigmann, Benno aut Hoffman, Arthur aut Rücknagel, Katrin aut Galle, Peter R. aut Neurath, Markus F. aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 57(2009), 5 vom: 20. Aug., Seite 369-376 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:57 year:2009 number:5 day:20 month:08 pages:369-376 https://dx.doi.org/10.1007/s00005-009-0046-5 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_65 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 57 2009 5 20 08 369-376 |
spelling |
10.1007/s00005-009-0046-5 doi (DE-627)SPR000040010 (SPR)s00005-009-0046-5-e DE-627 ger DE-627 rakwb eng Mudter, Jonas verfasserin aut IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. IRF4 (dpeaa)DE-He213 T cells (dpeaa)DE-He213 interferon regulatory factor (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 IL-17 (dpeaa)DE-He213 Yu, Jingling aut Amoussina, Lioubov aut Weigmann, Benno aut Hoffman, Arthur aut Rücknagel, Katrin aut Galle, Peter R. aut Neurath, Markus F. aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 57(2009), 5 vom: 20. Aug., Seite 369-376 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:57 year:2009 number:5 day:20 month:08 pages:369-376 https://dx.doi.org/10.1007/s00005-009-0046-5 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_65 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 57 2009 5 20 08 369-376 |
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10.1007/s00005-009-0046-5 doi (DE-627)SPR000040010 (SPR)s00005-009-0046-5-e DE-627 ger DE-627 rakwb eng Mudter, Jonas verfasserin aut IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. IRF4 (dpeaa)DE-He213 T cells (dpeaa)DE-He213 interferon regulatory factor (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 IL-17 (dpeaa)DE-He213 Yu, Jingling aut Amoussina, Lioubov aut Weigmann, Benno aut Hoffman, Arthur aut Rücknagel, Katrin aut Galle, Peter R. aut Neurath, Markus F. aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 57(2009), 5 vom: 20. Aug., Seite 369-376 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:57 year:2009 number:5 day:20 month:08 pages:369-376 https://dx.doi.org/10.1007/s00005-009-0046-5 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_65 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 57 2009 5 20 08 369-376 |
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10.1007/s00005-009-0046-5 doi (DE-627)SPR000040010 (SPR)s00005-009-0046-5-e DE-627 ger DE-627 rakwb eng Mudter, Jonas verfasserin aut IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. IRF4 (dpeaa)DE-He213 T cells (dpeaa)DE-He213 interferon regulatory factor (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 IL-17 (dpeaa)DE-He213 Yu, Jingling aut Amoussina, Lioubov aut Weigmann, Benno aut Hoffman, Arthur aut Rücknagel, Katrin aut Galle, Peter R. aut Neurath, Markus F. aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 57(2009), 5 vom: 20. Aug., Seite 369-376 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:57 year:2009 number:5 day:20 month:08 pages:369-376 https://dx.doi.org/10.1007/s00005-009-0046-5 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_65 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 57 2009 5 20 08 369-376 |
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10.1007/s00005-009-0046-5 doi (DE-627)SPR000040010 (SPR)s00005-009-0046-5-e DE-627 ger DE-627 rakwb eng Mudter, Jonas verfasserin aut IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. IRF4 (dpeaa)DE-He213 T cells (dpeaa)DE-He213 interferon regulatory factor (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 IL-17 (dpeaa)DE-He213 Yu, Jingling aut Amoussina, Lioubov aut Weigmann, Benno aut Hoffman, Arthur aut Rücknagel, Katrin aut Galle, Peter R. aut Neurath, Markus F. aut Enthalten in Archivum immunologiae et therapiae experimentalis [Cham (ZG)] : [Springer International Publishing AG], 1994 57(2009), 5 vom: 20. Aug., Seite 369-376 (DE-627)389872318 (DE-600)2149971-8 1661-4917 nnns volume:57 year:2009 number:5 day:20 month:08 pages:369-376 https://dx.doi.org/10.1007/s00005-009-0046-5 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_65 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_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 57 2009 5 20 08 369-376 |
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Mudter, Jonas @@aut@@ Yu, Jingling @@aut@@ Amoussina, Lioubov @@aut@@ Weigmann, Benno @@aut@@ Hoffman, Arthur @@aut@@ Rücknagel, Katrin @@aut@@ Galle, Peter R. @@aut@@ Neurath, Markus F. @@aut@@ |
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Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. 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Mudter, Jonas |
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Mudter, Jonas misc IRF4 misc T cells misc interferon regulatory factor misc IL-6 misc IL-17 IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation |
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IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation IRF4 (dpeaa)DE-He213 T cells (dpeaa)DE-He213 interferon regulatory factor (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 IL-17 (dpeaa)DE-He213 |
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IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation |
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Mudter, Jonas Yu, Jingling Amoussina, Lioubov Weigmann, Benno Hoffman, Arthur Rücknagel, Katrin Galle, Peter R. Neurath, Markus F. |
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irf4 selectively controls cytokine gene expression in chronic intestinal inflammation |
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IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation |
abstract |
Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 |
abstractGer |
Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 |
abstract_unstemmed |
Abstract The authors previously showed that interferon regulatory factor (IRF)4 knockout mice are protected from experimental oxazolone and TNBS colitis. Here the effect of IRF4 on the expression of pro- and anti-inflammatory cytokines in TNBS colitis and long-term $ CD45RB^{high} $ transfer colitis is examined. In TNBS colitis, no differences were found in interleukin (IL)-18 and tumor necrosis factor (TNF)-α expression between IRF4 knockout and wild-type mice. However, significant differences were detected in IL-6 and IL-17 production. Upon treatment with hyper-IL-6, $ IRF4^{–/–} $ mice lost their protective properties towards TNBS application. Hyper-IL-6 application induced IL-6 mRNA, but not IL-17 mRNA expression, suggesting that IL-6 deficiency is not primarily responsible for the lack of IL-17 production. T-bet and GATA-3 mRNA expressions were not affected upon IL-6 application. In transfer colitis, colonic cytokine mRNA analysis revealed a reduced production of IL-6 in $ IRF4^{–/–} $ reconstituted mice in the long-term course. In contrast, several other cytokines did not differ between the two groups (e.g. TNF-α and IL-10). Measurement of supernatants from splenic mononuclear cells revealed a significant difference in IL-6 and IL-17 production between the two groups. These findings suggest that IRF4 selectively regulates cytokine gene expression in chronic inflammation. IRF4 therefore emerges as an attractive target for the therapy of chronic intestinal inflammation. Blocking IRF4 might be an interesting option to modulate inflammation in the advanced state of inflammation. © L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2009 |
collection_details |
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container_issue |
5 |
title_short |
IRF4 selectively controls cytokine gene expression in chronic intestinal inflammation |
url |
https://dx.doi.org/10.1007/s00005-009-0046-5 |
remote_bool |
true |
author2 |
Yu, Jingling Amoussina, Lioubov Weigmann, Benno Hoffman, Arthur Rücknagel, Katrin Galle, Peter R. Neurath, Markus F. |
author2Str |
Yu, Jingling Amoussina, Lioubov Weigmann, Benno Hoffman, Arthur Rücknagel, Katrin Galle, Peter R. Neurath, Markus F. |
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doi_str |
10.1007/s00005-009-0046-5 |
up_date |
2024-07-03T13:38:53.795Z |
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|
score |
7.399637 |