ArticleiScience2025
IL-23 tunes inflammatory functions of human mucosal-associated invariant T cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Article
- Humans homozygous for rare or common hypomorphic IL23R variants are prone to tuberculosis.The Journal of experimental medicine · 2026Article
- Antigenic stimulation in conjunction with cytokine is required for mediating IL-17A production in human MAIT cells.Scientific reports · 2026Article
- Antigenic stimulation in conjunction with cytokine is required for mediating IL-17A production in human MAIT cells.bioRxiv : the preprint server for biology · 2026Article
- Interferon Regulatory Factors in Alcohol-Associated Liver Disease: Cell-Type Programs, Danger Signaling, and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- IL-23 and monocyte interactions redirect human Th17.1 cells to an IL-17AFrontiers in immunology · 2026Article
- Mucosal-Associated Invariant T Cells: Origins, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- RELA Haploinsufficiency Manifesting as an Atypical Phenotype of Crohn's Disease.Inflammatory bowel diseases · 2025Article
- Control of MAIT cell functions by cytokines in health and disease.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-23 signaling plays a key role in the pathogenesis of chronic inflammatory and infectious diseases, yet the cellular targets and signaling pathways affected by this cytokine remain poorly understood. We show that IL-23 receptors are expressed on the large majority of human mucosal-associated invariant T (MAIT), but not of conventional T cells. Protein and transcriptional profiling at the population and single cell level demonstrates that stimulation with IL-23 or the structurally related cytokine IL-12 drives distinct functional profiles, revealing a high level of plasticity of MAIT cells. IL-23, in particular, affects key molecules and pathways related to autoimmunity and cytotoxic functions. Integrated analysis of transcriptomes and chromatin accessibility, supported by CRISPR-Cas9 mediated deletion, shows that AP-1 transcription factors constitute a key regulatory node of the IL-23 pathway in MAIT cells. In conclusion, our findings indicate that MAIT cells are key mediators of IL-23 functions in immunity to infections and chronic inflammatory diseases.
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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.