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

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...

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Published inCell death & disease Vol. 12; no. 5; p. 431
Main Authors Guan, Di, Wang, Zixi, Huo, Jianxin, Xu, Shengli, Lam, Kong-Peng
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 30.04.2021
Springer Nature B.V
Nature Publishing Group
Subjects
13/106
13/21
13/31
38/22
38/23
38/77
631/250/249/2510/257
631/250/256
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64/110
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Antibodies
Biochemistry
Biomedical and Life Sciences
Bruton's tyrosine kinase
Cell Biology
Cell Culture
Colitis
Dendritic cells
Digestive system
Gastrointestinal tract
Homeostasis
Immune system
Immunology
Inflammatory bowel disease
Inflammatory bowel diseases
Interleukin 12
Intestinal microflora
Intestine
Kinases
Life Sciences
Lymphocytes T
Microbiota
Protein-tyrosine kinase
Risk factors
Rodents
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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.
AbstractList 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 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.
ArticleNumber 431
Author Guan, Di
Huo, Jianxin
Xu, Shengli
Wang, Zixi
Lam, Kong-Peng
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  organization: NUS Graduate School for Integrative Sciences & Engineering (NGS), National University of Singapore, Bioprocessing Technology Institute, ASTAR (Agency for Science, Technology and Research), Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Immunology Network (SIgN), ASTAR (Agency for Science, Technology and Research)
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SSID ssj0000330256
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Snippet Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase (BTK) is...
Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton's tyrosine kinase (BTK) is...
Abstract Inflammatory bowel disease (IBD) is driven by multiple genetic and environmental risk factors. Patients with mutations in Bruton’s tyrosine kinase...
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Antibodies
Biochemistry
Biomedical and Life Sciences
Bruton's tyrosine kinase
Cell Biology
Cell Culture
Colitis
Dendritic cells
Digestive system
Gastrointestinal tract
Homeostasis
Immune system
Immunology
Inflammatory bowel disease
Inflammatory bowel diseases
Interleukin 12
Intestinal microflora
Intestine
Kinases
Life Sciences
Lymphocytes T
Microbiota
Protein-tyrosine kinase
Risk factors
Rodents
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Title Bruton’s tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response
URI https://link.springer.com/article/10.1038/s41419-021-03702-y
https://www.ncbi.nlm.nih.gov/pubmed/33931590
https://www.proquest.com/docview/2520052558
https://search.proquest.com/docview/2520871290
https://pubmed.ncbi.nlm.nih.gov/PMC8087775
https://doaj.org/article/9bdc3c983c534270a4bd25ff43292385
Volume 12
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