ArticleEuropean journal of immunology2015
Human group3 innate lymphoid cells express DR3 and respond to TL1A with enhanced IL-22 production and IL-2-dependent proliferation.
Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 53 citations in OpenAlex.
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- Article
- Therapeutic Potential of Tulisokibart and Anti-TL1A Therapy in Inflammatory Disorders: Current Insights and Future Directions.Clinical reviews in allergy & immunology · 2026Review
- Article
- The Therapeutic Potential of Targeting TL1A in a Spectrum of Inflammatory Disorders.Journal of inflammation research · 2026Review
- Review
- Review
- Innate lymphoid cells in the spotlight: from biomarkers to blueprint for innovative immunotherapy.Frontiers in immunology · 2025Review
- Versatile roles of innate lymphoid cells at the mucosal barrier: from homeostasis to pathological inflammation.Experimental & molecular medicine · 2023Review
- Review
- Group 3 innate lymphoid cells secret neutrophil chemoattractants and are insensitive to glucocorticoid via aberrant GR phosphorylation.Respiratory research · 2023Article
- Microbiota as key factors in inflammatory bowel disease.Frontiers in microbiology · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Role of TL1A in Inflammatory Autoimmune Diseases: A Comprehensive Review.Frontiers in immunology · 2022Review
- Therapeutic manipulation of innate lymphoid cells.JCI insight · 2021Review
- EfficientFrontiers in immunology · 2021Article
- Modulation of Intestinal ILC3 for the Treatment of Type 1 Diabetes.Frontiers in immunology · 2021Review
- ILC3, a Central Innate Immune Component of the Gut-Brain Axis in Multiple Sclerosis.Frontiers in immunology · 2021Review
- DR3 stimulation of adipose resident ILC2s ameliorates type 2 diabetes mellitus.Nature communications · 2020Article
- Innate lymphoid cells link gut microbes with mucosal T cell immunity.Gut microbes · 2020Review
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 2 institutions in 2 countries.
Funding
Abstract
Death receptor 3 (DR3, TNFRSF25) is expressed by activated lymphocytes and signaling by its ligand, TL1A, enhances cytokine expression and proliferation. Recent studies show that DR3 is also present on murine type 2 innate lymphoid cells (ILC2s). Here, we show that DR3 is expressed by IL-22-producing human group 3 innate lymphoid cells (ILC3s). Stimulation of ILC3s with exogenous TL1A alone had no impact on cytokine production or proliferation. Addition of TL1A to IL-1β + IL-23 significantly enhanced the amount IL-22 produced by ILC3s as well as the percentage IL-22- and IL-8-producing cells. Addition of TL1A to IL-1β + IL-23 also augmented ILC3 proliferation. Mechanistically, this occurred through the upregulation of CD25 and responsiveness to IL-2 stimulation. The combination of TL1A, IL-1β+ IL-23, and IL-2 expanded ILC3s while IL-1β+ IL-23 did not increase proliferation above controls. After 2 weeks of expansion, ILC3s maintained their phenotype, transcription factor expression, and function (IL-22 production). These findings identify DR3 as a costimulatory molecule on ILC3s that could be exploited for ex vivo expansion and clinical use.
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.