ReviewImmunology2008
The role of T-regulatory cells and Toll-like receptors in the pathogenesis of human inflammatory bowel disease.
Review in Immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 152 citations in OpenAlex.
- Oral mixture of autologous colon-extracted proteins for the Crohn's disease: A double-blind trial.World journal of gastroenterology · 2015Trial
- Review
- Rice bran extract ameliorates experimental colitis by modulating gut dysbiosis and toll-like receptor 4/nuclear factor kappa β signaling.Indian journal of pharmacology · 2026Article
- Opportunities and challenges harnessing antigen-specific CD4+ regulatory T cells in inflammatory bowel disease.Frontiers in immunology · 2025Review
- Development of Ulcerative Colitis in a Patient With Human Immunodeficiency Virus.Case reports in gastrointestinal medicine · 2025Article
- Single-cell multi-ome and immune profiles of the Inspiration4 crew reveal conserved, cell-type, and sex-specific responses to spaceflight.Nature communications · 2024Article
- Immune response modulation in inflammatory bowel diseases byWorld journal of gastroenterology · 2023Review
- Protective Effect of NovelMicroorganisms · 2023Article
- Inhibition of IRAK 1/4 alleviates colitis by inhibiting TLR4/ NF-κB pathway and protecting the intestinal barrier.Bosnian journal of basic medical sciences · 2022Article
- TLR4 regulates RORγtMicrobiome · 2022Article
- Beneficial Effects of Celastrol on Immune Balance by Modulating Gut Microbiota in Experimental Ulcerative Colitis Mice.Genomics, proteomics & bioinformatics · 2022Article
- Role of Toll-Like Receptor 5 in the Development of Ulcerative Colitis.Archives of Razi Institute · 2021Article
- Microbiome-Mediated Immune Signaling in Inflammatory Bowel Disease and Colorectal Cancer: Support From Meta-omics Data.Frontiers in cell and developmental biology · 2021Review
- Toll Like Receptors as Sensors of the Tumor Microbial Dysbiosis: Implications in Cancer Progression.Frontiers in cell and developmental biology · 2021Review
- JAK-STAT pathway targeting for the treatment of inflammatory bowel disease.Nature reviews. Gastroenterology & hepatology · 2020Review
- Review
- EngineeredMicroorganisms · 2019Article
- Toll-like receptor 6 expression, sequence variants, and their association with colorectal cancer risk.Journal of Cancer · 2019Article
- PD-L1 is required for human endometrial regenerative cells-associated attenuation of experimental colitis in mice.American journal of translational research · 2019Article
- A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease.Journal of immunology research · 2019Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two related chronic inflammatory diseases, Crohn's disease and ulcerative colitis, are together often referred to as inflammatory bowel disease (IBD). Current treatment options are not curative, and patients face lifelong therapy and debilitation. IBD is thought to be the product of a combination of genetic and environmental factors that result in the abnormal regulation of immune responses. Experimental models have demonstrated that normal CD4+ T-regulatory (Treg) cell responses and commensal bacteria are required for the maintenance of gut immune homeostasis. Recent evidence that CD4+ T cells express Toll-like receptors (TLRs) and respond directly to TLR ligands, suggests that signals from commensal bacteria may directly affect T-cell responses in the gut. In this review, we focus on evidence that defects in Treg cells may underlie IBD in humans. In addition, we discuss evidence that direct signaling via TLRs to T cells can affect IBD and that T-cell-dependent responses to bacterial proteins, such as flagellin, are central to the aetiology of this disease.
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What OpenQuestion holds
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.