IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish

MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immun...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Xiaolong Yan [verfasserIn] Xueyan Zhao [verfasserIn] Ruixuan Huo [verfasserIn] Tianjun Xu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	MyD88 IRF3 IRF8 NF-κB ubiquitination

Übergeordnetes Werk:	In: Frontiers in Immunology - Frontiers Media S.A., 2011, 11(2020)
Übergeordnetes Werk:	volume:11 ; year:2020

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fimmu.2020.00606

Katalog-ID:	DOAJ049882422

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520			\|a MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system.
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allfields	10.3389/fimmu.2020.00606 doi (DE-627)DOAJ049882422 (DE-599)DOAJd33adca7330f46a483eef5081e87cf7a DE-627 ger DE-627 rakwb eng RC581-607 Xiaolong Yan verfasserin aut IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system. MyD88 IRF3 IRF8 NF-κB ubiquitination Immunologic diseases. Allergy Xiaolong Yan verfasserin aut Xueyan Zhao verfasserin aut Ruixuan Huo verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 11(2020) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:11 year:2020 https://doi.org/10.3389/fimmu.2020.00606 kostenfrei https://doaj.org/article/d33adca7330f46a483eef5081e87cf7a kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2020.00606/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020
spelling	10.3389/fimmu.2020.00606 doi (DE-627)DOAJ049882422 (DE-599)DOAJd33adca7330f46a483eef5081e87cf7a DE-627 ger DE-627 rakwb eng RC581-607 Xiaolong Yan verfasserin aut IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system. MyD88 IRF3 IRF8 NF-κB ubiquitination Immunologic diseases. Allergy Xiaolong Yan verfasserin aut Xueyan Zhao verfasserin aut Ruixuan Huo verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 11(2020) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:11 year:2020 https://doi.org/10.3389/fimmu.2020.00606 kostenfrei https://doaj.org/article/d33adca7330f46a483eef5081e87cf7a kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2020.00606/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020
allfields_unstemmed	10.3389/fimmu.2020.00606 doi (DE-627)DOAJ049882422 (DE-599)DOAJd33adca7330f46a483eef5081e87cf7a DE-627 ger DE-627 rakwb eng RC581-607 Xiaolong Yan verfasserin aut IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system. MyD88 IRF3 IRF8 NF-κB ubiquitination Immunologic diseases. Allergy Xiaolong Yan verfasserin aut Xueyan Zhao verfasserin aut Ruixuan Huo verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 11(2020) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:11 year:2020 https://doi.org/10.3389/fimmu.2020.00606 kostenfrei https://doaj.org/article/d33adca7330f46a483eef5081e87cf7a kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2020.00606/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020
allfieldsGer	10.3389/fimmu.2020.00606 doi (DE-627)DOAJ049882422 (DE-599)DOAJd33adca7330f46a483eef5081e87cf7a DE-627 ger DE-627 rakwb eng RC581-607 Xiaolong Yan verfasserin aut IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system. MyD88 IRF3 IRF8 NF-κB ubiquitination Immunologic diseases. Allergy Xiaolong Yan verfasserin aut Xueyan Zhao verfasserin aut Ruixuan Huo verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 11(2020) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:11 year:2020 https://doi.org/10.3389/fimmu.2020.00606 kostenfrei https://doaj.org/article/d33adca7330f46a483eef5081e87cf7a kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2020.00606/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020
allfieldsSound	10.3389/fimmu.2020.00606 doi (DE-627)DOAJ049882422 (DE-599)DOAJd33adca7330f46a483eef5081e87cf7a DE-627 ger DE-627 rakwb eng RC581-607 Xiaolong Yan verfasserin aut IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system. MyD88 IRF3 IRF8 NF-κB ubiquitination Immunologic diseases. Allergy Xiaolong Yan verfasserin aut Xueyan Zhao verfasserin aut Ruixuan Huo verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut Tianjun Xu verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 11(2020) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:11 year:2020 https://doi.org/10.3389/fimmu.2020.00606 kostenfrei https://doaj.org/article/d33adca7330f46a483eef5081e87cf7a kostenfrei https://www.frontiersin.org/article/10.3389/fimmu.2020.00606/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020
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authorswithroles_txt_mv	Xiaolong Yan @@aut@@ Xueyan Zhao @@aut@@ Ruixuan Huo @@aut@@ Tianjun Xu @@aut@@
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callnumber-first	R - Medicine
author	Xiaolong Yan
spellingShingle	Xiaolong Yan misc RC581-607 misc MyD88 misc IRF3 misc IRF8 misc NF-κB misc ubiquitination misc Immunologic diseases. Allergy IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish
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topic_title	RC581-607 IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish MyD88 IRF3 IRF8 NF-κB ubiquitination
topic	misc RC581-607 misc MyD88 misc IRF3 misc IRF8 misc NF-κB misc ubiquitination misc Immunologic diseases. Allergy
topic_unstemmed	misc RC581-607 misc MyD88 misc IRF3 misc IRF8 misc NF-κB misc ubiquitination misc Immunologic diseases. Allergy
topic_browse	misc RC581-607 misc MyD88 misc IRF3 misc IRF8 misc NF-κB misc ubiquitination misc Immunologic diseases. Allergy
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title	IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish
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title_full	IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish
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title_sort	irf3 and irf8 regulate nf-κb signaling by targeting myd88 in teleost fish
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title_auth	IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish
abstract	MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system.
abstractGer	MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system.
abstract_unstemmed	MyD88 is a conserved intracellular adaptor, which plays an important role in the innate immune system. MyD88 transmits signals for downstream of toll-like and IL-1 receptors to activate NF-κB signaling pathway, which is tightly controlled in the immune response to maintain immune intensity and immune homeostasis at different stages. NF-κB signaling pathway has been extensively studied in mammals, but regulatory molecular mechanism is still unclear in teleost fish. We determined that IRF3 and IRF8 can regulate MyD88-mediated NF-κB signaling pathway in fish. Interestingly, MyD88 is precisely regulated by IRF3 and IRF8 through the same mechanism but in completely opposite ways. IRF3 promotes MyD88-mediated NF-κB signaling pathway, whereas IRF8 inhibits the signaling pathway. MyD88 is regulated via ubiquitin–proteasome degradation, whereas IRF3 or IRF8 inhibited or promoted MyD88 degradation in this pathway. Specifically, in the early stage of lipopolysaccharide (LPS) stimulation or Vibrio infection, up-regulation of IRF3 and down-regulation of IRF8 eventually increased MyD88 expression to activate the NF-κB signaling pathway to trigger immune response. In the late stage of stimulation, down-regulated IRF3 and up-regulated IRF8 synergistically regulate the expression of MyD88 to a normal level, thus maintaining the immune balance of homeostasis and preventing serious damage from persistent over-immunization. This study presents information on Myd88–NF-κB signaling pathway in teleost fish and provides new insights into its regulatory mechanism in fish immune system.
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title_short	IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish
url	https://doi.org/10.3389/fimmu.2020.00606 https://doaj.org/article/d33adca7330f46a483eef5081e87cf7a https://www.frontiersin.org/article/10.3389/fimmu.2020.00606/full https://doaj.org/toc/1664-3224
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up_date	2024-07-04T01:11:38.270Z
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IRF3 and IRF8 Regulate NF-κB Signaling by Targeting MyD88 in Teleost Fish

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