Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response

Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptor...
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Autor*in:	Di Guan [verfasserIn] Zixi Wang [verfasserIn] Jianxin Huo [verfasserIn] Shengli Xu [verfasserIn] Kong-Peng Lam [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Übergeordnetes Werk:	In: Cell Death and Disease - Nature Publishing Group, 2010, 12(2021), 5, Seite 15
Übergeordnetes Werk:	volume:12 ; year:2021 ; number:5 ; pages:15

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1038/s41419-021-03702-y

Katalog-ID:	DOAJ055040012

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520			\|a Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization.
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allfields	10.1038/s41419-021-03702-y doi (DE-627)DOAJ055040012 (DE-599)DOAJ9bdc3c983c534270a4bd25ff43292385 DE-627 ger DE-627 rakwb eng QH573-671 Di Guan verfasserin aut Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization. Cytology Zixi Wang verfasserin aut Jianxin Huo verfasserin aut Shengli Xu verfasserin aut Kong-Peng Lam verfasserin aut In Cell Death and Disease Nature Publishing Group, 2010 12(2021), 5, Seite 15 (DE-627)620145250 (DE-600)2541626-1 20414889 nnns volume:12 year:2021 number:5 pages:15 https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/article/9bdc3c983c534270a4bd25ff43292385 kostenfrei https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/toc/2041-4889 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 12 2021 5 15
spelling	10.1038/s41419-021-03702-y doi (DE-627)DOAJ055040012 (DE-599)DOAJ9bdc3c983c534270a4bd25ff43292385 DE-627 ger DE-627 rakwb eng QH573-671 Di Guan verfasserin aut Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization. Cytology Zixi Wang verfasserin aut Jianxin Huo verfasserin aut Shengli Xu verfasserin aut Kong-Peng Lam verfasserin aut In Cell Death and Disease Nature Publishing Group, 2010 12(2021), 5, Seite 15 (DE-627)620145250 (DE-600)2541626-1 20414889 nnns volume:12 year:2021 number:5 pages:15 https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/article/9bdc3c983c534270a4bd25ff43292385 kostenfrei https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/toc/2041-4889 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 12 2021 5 15
allfields_unstemmed	10.1038/s41419-021-03702-y doi (DE-627)DOAJ055040012 (DE-599)DOAJ9bdc3c983c534270a4bd25ff43292385 DE-627 ger DE-627 rakwb eng QH573-671 Di Guan verfasserin aut Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization. Cytology Zixi Wang verfasserin aut Jianxin Huo verfasserin aut Shengli Xu verfasserin aut Kong-Peng Lam verfasserin aut In Cell Death and Disease Nature Publishing Group, 2010 12(2021), 5, Seite 15 (DE-627)620145250 (DE-600)2541626-1 20414889 nnns volume:12 year:2021 number:5 pages:15 https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/article/9bdc3c983c534270a4bd25ff43292385 kostenfrei https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/toc/2041-4889 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 12 2021 5 15
allfieldsGer	10.1038/s41419-021-03702-y doi (DE-627)DOAJ055040012 (DE-599)DOAJ9bdc3c983c534270a4bd25ff43292385 DE-627 ger DE-627 rakwb eng QH573-671 Di Guan verfasserin aut Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization. Cytology Zixi Wang verfasserin aut Jianxin Huo verfasserin aut Shengli Xu verfasserin aut Kong-Peng Lam verfasserin aut In Cell Death and Disease Nature Publishing Group, 2010 12(2021), 5, Seite 15 (DE-627)620145250 (DE-600)2541626-1 20414889 nnns volume:12 year:2021 number:5 pages:15 https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/article/9bdc3c983c534270a4bd25ff43292385 kostenfrei https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/toc/2041-4889 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 12 2021 5 15
allfieldsSound	10.1038/s41419-021-03702-y doi (DE-627)DOAJ055040012 (DE-599)DOAJ9bdc3c983c534270a4bd25ff43292385 DE-627 ger DE-627 rakwb eng QH573-671 Di Guan verfasserin aut Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization. Cytology Zixi Wang verfasserin aut Jianxin Huo verfasserin aut Shengli Xu verfasserin aut Kong-Peng Lam verfasserin aut In Cell Death and Disease Nature Publishing Group, 2010 12(2021), 5, Seite 15 (DE-627)620145250 (DE-600)2541626-1 20414889 nnns volume:12 year:2021 number:5 pages:15 https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/article/9bdc3c983c534270a4bd25ff43292385 kostenfrei https://doi.org/10.1038/s41419-021-03702-y kostenfrei https://doaj.org/toc/2041-4889 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 12 2021 5 15
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source	In Cell Death and Disease 12(2021), 5, Seite 15 volume:12 year:2021 number:5 pages:15
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topic_title	QH573-671 Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response
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title	Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response
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title_full	Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response
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title_sort	bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating th1 response
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title_auth	Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response
abstract	Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization.
abstractGer	Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization.
abstract_unstemmed	Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is known to manifest high prevalence of intestinal disorders including IBD. Although BTK mediates the signaling of various immune receptors, little is known how BTK maintains the homeostasis of the gut immune system. Here, we show that BTK-deficiency promotes IBD progression in a mouse model of colitis. Interestingly, the increased colitis susceptibility of BTK-deficient mice is not caused by gut microbiota changes but rather arises from enhanced pro-inflammatory Th1 response. More importantly, we find the heightened Th1 response in BTK-deficient mice to result from both T cell-extrinsic and -intrinsic mechanisms. BTK-deficient dendritic cells secret elevated levels of the Th1-polarizing cytokine IL-12 and BTK-deficient T cells are inherently more prone to Th1 differentiation. Thus, BTK plays critical roles in maintaining gut immune homeostasis and preventing inflammation via regulating T-cell polarization.
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title_short	Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response
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