ArticlePloS one2014
Selective accumulation of pro-inflammatory T cells in the intestine contributes to the resistance to autoimmune demyelinating disease.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- FFAR2 activation induces IL-22-dependent intestinal immune responses to suppress CNS autoimmunity.EMBO molecular medicine · 2026Article
- The gut microbiota-miRNA axis in multiple sclerosis: Mechanisms and therapeutic potentials.Folia microbiologica · 2026Review
- Systemic microbial antigen administration ameliorates experimental autoimmune encephalomyelitis via MHC-II downregulation in the CNS and secondary lymphoid organs.Journal of neuropathology and experimental neurology · 2026Article
- Article
- Increased regulatory activity of intestinal innate lymphoid cells type 3 (ILC3) prevents experimental autoimmune encephalomyelitis severity.Journal of neuroinflammation · 2024Article
- Review
- Sepsis and multiple sclerosis: Causative links and outcomes.Immunology letters · 2021Review
- Targeting the gut to treat multiple sclerosis.The Journal of clinical investigation · 2021Review
- The Nerves to Conduct a Multiple Sclerosis Crime Investigation.International journal of molecular sciences · 2021Review
- ILC3, a Central Innate Immune Component of the Gut-Brain Axis in Multiple Sclerosis.Frontiers in immunology · 2021Review
- IL-17 and CCR9Frontiers in immunology · 2021Article
- Blocking integrin αJournal of hepatology · 2020Article
- Microbiome in Multiple Sclerosis; Where Are We, What We Know and Do Not Know.Brain sciences · 2020Review
- Fecal Microbiota Transplantation in Neurological Disorders.Frontiers in cellular and infection microbiology · 2020Review
- Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats.Scientific reports · 2019Article
- Microbial monotherapy withExpert review of neurotherapeutics · 2019Review
- Experimental Autoimmune Encephalomyelitis (EAE) as Animal Models of Multiple Sclerosis (MS).Cold Spring Harbor perspectives in medicine · 2018Review
- The intestinal barrier in multiple sclerosis: implications for pathophysiology and therapeutics.Brain : a journal of neurology · 2018Review
- Mechanisms of T cell organotropism.Cellular and molecular life sciences : CMLS · 2016Review
- Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats.Frontiers in microbiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin-specific, pro-inflammatory TH17 cells are widely regarded as the drivers of experimental autoimmune encephalomyelitis (EAE), an animal model for Multiple sclerosis (MS). The factors, responsible for the generation and maintenance of TH17 cells as well as their participation in the pathogenic cascade leading to the demyelinating disease, have been studied extensively. However, how these harmful autoreactive cells are controlled in vivo remains unclear. By comparing TCR transgenic mice on a disease susceptible and a disease resistant genetic background, we show here that pathogenic TH17 cells are sequestered within the intestine of spontaneous EAE resistant B10.S mice. Disease resistant B10.S mice harbored higher frequencies of TH17 cells in the intestine compared to EAE susceptible SJL/J mice. Moreover, transferred TH17 cells selectively migrated to intestinal lymphoid organs of B10.S mice. The sequestration of TH17 cells in the gut was partially dependent on the gut homing receptor α4β7-mediated adhesion to the intestine. Administration of α4β7 blocking-antibodies increased the peripheral availability of TH17 cells, resulting in increased EAE severity after immunization in B10.S mice. Together, these results support the concept that the intestine is a check-point for controlling pathogenic, organ-specific T cells.
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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.