ArticleGut2001
Role of T lymphocytes in rat 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis: increased mortality after gammadelta T cell depletion and no effect of alphabeta T cell depletion.
Article in Gut, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
- Crosstalk between the microbiota and intestinal γδ T cell compartments in health and IBD.Gut microbes · 2026Review
- Similarities and Differences in the Immune Characteristics of Intestinal Gamma Delta T Cells From Patients With Crohn's Disease and Ulcerative Colitis and Their Correlation With Disease Activity.Immunity, inflammation and disease · 2025Article
- Mucosal Responses to Type II Interferon in IBD.Inflammatory bowel diseases · 2025Article
- Intestinal CD8+ γδ T cells shift from immune activation to suppression, with concomitant impairment of cytotoxicity as disease activity increases in patients with ulcerative colitis.Central-European journal of immunology · 2025Article
- Elevated levels of IRF1 and CASP1 as pyroptosis-related biomarkers for intestinal epithelial cells in Crohn's disease.Frontiers in immunology · 2025Article
- γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023Review
- Development and function of natural TCRFrontiers in immunology · 2022Review
- Inflammatory Bowel Diseases: It's Time for the Adenosine System.Frontiers in immunology · 2020Article
- DeSUMOylase SENP7-Mediated Epithelial Signaling Triggers Intestinal Inflammation via Expansion of Gamma-Delta T Cells.Cell reports · 2019Article
- γδ T Cells: Crosstalk Between Microbiota, Chronic Inflammation, and Colorectal Cancer.Frontiers in immunology · 2018Review
- Dominant Negative FADD/MORT1 Inhibits the Development of Intestinal Intraepithelial Lymphocytes With a Marked Defect on CD8αα+TCRγδ+ T Cells.Frontiers in immunology · 2018Article
- Sentinels at the frontline: the role of intraepithelial lymphocytes in inflammatory bowel disease.Current pharmacology reports · 2017Article
- Immunophenotype of Peripheral Blood Lymphocytes in Dogs with Inflammatory Bowel Disease.Journal of veterinary internal medicine · 2017Article
- Intestinal Barrier Interactions with Specialized CD8 T Cells.Frontiers in immunology · 2017Review
- Cytokine Networks and T-Cell Subsets in Inflammatory Bowel Diseases.Inflammatory bowel diseases · 2016Review
- All hands on DE(T)C: Epithelial-resident γδ T cells respond to tissue injury.Cellular immunology · 2015Review
- Interleukin 23 in Crohn's disease.Inflammatory bowel diseases · 2014Review
- Recognition of gut microbiota by NOD2 is essential for the homeostasis of intestinal intraepithelial lymphocytes.The Journal of experimental medicine · 2013Article
- Skin- and gut-homing molecules on human circulating γδ T cells and their dysregulation in inflammatory bowel disease.Clinical and experimental immunology · 2012Article
- Gut mucosal injury in neonates is marked by macrophage infiltration in contrast to pleomorphic infiltrates in adult: evidence from an animal model.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimIndirect evidence suggests that CD4+ T cells have a pathogenic while gammadelta T cells have a protective role in the initiation and perpetuation of inflammatory bowel disease. To define the role of T cell subsets in a rat colitis model (2,4,6-trinitrobenzene sulphonic acid (TNBS)) we analysed colitis severity after effective depletion of T helper cells, alphabeta T cells, or gammadelta T cells.
methodsT helper cells, alphabeta T cells, or gammadelta T cells were depleted using previously described monoclonal antibodies directed at the CD4 molecule (OX38), the CD2 molecule (OX34, both depleting CD4+ T cells), the alphabeta T cell receptor (R73), and the gammadelta T cell receptor (V65). Depletion was verified by flow cytometry and/or immunohistology. Colitis was induced using intracolonic application of TNBS.
resultsSurprisingly, depletion of T helper cells or alphabeta T cells had no influence on survival, macroscopic or microscopic scores, or myeloperoxidase activity following colitis induction. In contrast, depletion of gammadelta T cells resulted in significantly increased mortality (V65: 73%, n=15) compared with controls (30%, n=13; p<0.03). In addition, colitis was histologically more severe in the gammadelta T cell depleted group compared with controls (p<0.05).
conclusionsT helper cells or alphabeta T cells did not influence the initiation or perpetuation of rat TNBS colitis. In contrast, gammadelta T cells had a protective role in rat TNBS colitis as depletion caused increased mortality.
Indexed as
Identifiers
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.