ArticleGut microbes
Role of SFB in autoimmune arthritis: an example of regulation of autoreactive T cell sensitivity in the gut.
Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Causal relationship between gut microbiota and type 2 diabetes: a two-sample Mendelian randomization study.Frontiers in microbiology · 2023Article
- Genetically Predicted Causality of 28 Gut Microbiome Families and Type 2 Diabetes Mellitus Risk.Frontiers in endocrinology · 2022Article
- Distribution and Strain Diversity of Immunoregulating Segmented Filamentous Bacteria in Human Intestinal Lavage Samples.Microbial ecology · 2020Article
- Visions of Eye Commensals: The Known and the Unknown About How the Microbiome Affects Eye Disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018Review
- The Gut Microbiome and Multiple Sclerosis.Cold Spring Harbor perspectives in medicine · 2018Review
- The influence of gut-derived CD39 regulatory T cells in CNS demyelinating disease.Translational research : the journal of laboratory and clinical medicine · 2017Review
- PCR detection of segmented filamentous bacteria in the terminal ileum of patients with ulcerative colitis.BMJ open gastroenterology · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A key role for segmented filamentous bacteria (SFB) has recently been demonstrated in several mouse models of autoimmune diseases, including autoimmune arthritis and multiple sclerosis. The mechanism governing the activation of systemic autoreactive T cell responses by such commensals in the gut, however, remained elusive. In this addendum, we discuss recent results addressing the local regulation of autoreactive T cell sensitivity by these unique bacteria. We found that the presence of SFB in the gut microbiota was sufficient to promote a local inflammatory microenvironment altering the T cell-intrinsic desensitization process normally occurring in response to chronic self-antigen stimulation. In the absence of this key tolerance checkpoint, sustained chronic T cell proliferation, IFNγ production, and B cell activation eventually led to the development of enhanced pathologies in a Th1-driven T cell-transfer model of autoimmune arthritis.
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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.