ArticleNature communications2016
T-bet is a key modulator of IL-23-driven pathogenic CD4(+) T cell responses in the intestine.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 83 citations in OpenAlex.
- A temporal differentiation program after birth delineates γδ T cell immunity.Science advances · 2026Article
- Effect of the intestinal microbiota on TSeminars in immunopathology · 2026Review
- Unraveling the role of IL-17 signaling pathway in breast cancer-related depression: insights from in vivo/in vitro models and transcriptomic analysis.Functional & integrative genomics · 2026Article
- Single-cell multiomics reveals macrophage-derived IL-23 and CXCL9/10 drive pathogenic IFNGJournal for immunotherapy of cancer · 2025Article
- Metabolic Stress Expands Polyfunctional, Proinflammatory ThArthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Aryl Hydrocarbon Receptor Activation Promotes Effector CD4+ T Cell Homeostasis and Restrains Salt-Sensitive Hypertension.Function (Oxford, England) · 2025Article
- Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells.Cellular & molecular immunology · 2024Review
- HIF-2α-dependent induction of miR-29a restrains TNature communications · 2024Article
- Hybrid lineages of CD4Frontiers in immunology · 2024Review
- A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation.bioRxiv : the preprint server for biology · 2023Article
- The Absence of IL-12Rβ2 Expression on Recipient Nonhematopoietic Cells Diminishes Acute Graft-versus-Host Disease in the Gastrointestinal Tract.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Methylation ofGenes · 2022Article
- A systematic comparison of FOSL1, FOSL2 and BATF-mediated transcriptional regulation during early human Th17 differentiation.Nucleic acids research · 2022Article
- Autoreactive memory Th17 cells are principally derived from T-betJournal of autoimmunity · 2022Article
- A population of naive-like CD4European journal of immunology · 2022Article
- Th17 cell plasticity towards a T-bet-dependent Th1 phenotype is required for bacterial control in Staphylococcus aureus infection.PLoS pathogens · 2022Article
- GDF15 Suppresses Lymphoproliferation and Humoral Autoimmunity in a Murine Model of Systemic Lupus Erythematosus.Journal of innate immunity · 2022Article
- Article
- Removal of CD276Bone marrow transplantation · 2021Article
- T-helper 22 cells develop as a distinct lineage from Th17 cells during bacterial infection and phenotypic stability is regulated by T-bet.Mucosal immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
IL-23 is a key driver of pathogenic Th17 cell responses. It has been suggested that the transcription factor T-bet is required to facilitate IL-23-driven pathogenic effector functions; however, the precise role of T-bet in intestinal T cell responses remains elusive. Here, we show that T-bet expression by T cells is not required for the induction of colitis or the differentiation of pathogenic Th17 cells but modifies qualitative features of the IL-23-driven colitogenic response by negatively regulating IL-23R expression. Consequently, absence of T-bet leads to unrestrained Th17 cell differentiation and activation characterized by high amounts of IL-17A and IL-22. The combined increase in IL-17A/IL-22 results in enhanced epithelial cell activation and inhibition of either IL-17A or IL-22 leads to disease amelioration. Our study identifies T-bet as a key modulator of IL-23-driven colitogenic responses in the intestine and has important implications for understanding of heterogeneity among inflammatory bowel disease patients.
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.