ArticleCell death & disease2021
Bruton's tyrosine kinase regulates gut immune homeostasis through attenuating Th1 response.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Safety and efficacy of different JAK inhibitors in the treatment of inflammatory bowel disease: a network meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Exploring the mechanism of Qinlian Yuyang Decoction in the treatment of ulcerative colitis based on multi-omics technology.Chinese medicine · 2026Article
- Purified diet reduces intestinal IgA and alters the microbiota accordingly.The British journal of nutrition · 2026Article
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
- Neuroimmune interactions: The bridge between inflammatory bowel disease and the gut microbiota.Clinical and translational medicine · 2025Review
- Investigating the molecular mechanisms underlying the co-occurrence of Parkinson's disease and inflammatory bowel disease through the integration of multiple datasets.Scientific reports · 2024Article
- Chronic Lymphocytic Leukemia: Management of Adverse Events in the Era of Targeted Agents.Cancers · 2024Review
- Exploring the common mechanism of vascular dementia and inflammatory bowel disease: a bioinformatics-based study.Frontiers in immunology · 2024Article
- IgA Determines Bacterial Composition in the Gut.Crohn's & colitis 360 · 2023Article
- Bruton's Tyrosine Kinase Supports Gut Mucosal Immunity and Commensal Microbiome Recognition in Autoimmune Arthritis.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.