ArticleNature2016
Glial-cell-derived neuroregulators control type 3 innate lymphoid cells and gut defence.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 1 of them a synthesis that pooled it.
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
213 citing papers in PubMed, 1 synthesis or guideline pooled it, 344 citations in OpenAlex.
- Global research status and trends of enteric glia: a bibliometric analysis.Frontiers in pharmacology · 2024Pooled it
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- The interaction of enteric glial cells and gut microbiota in health and diseases.Science China. Life sciences · 2026Article
- γδ T Cell-Mediated Neuroimmune Interactions in Skin Inflammation and Allergy.Clinical reviews in allergy & immunology · 2026Review
- Current Perspectives on the Inflammatory Bowel Disease Pathogenesis of Microbiota and the Gut-Brain Axis, and Emerging Therapeutics.Biomedicines · 2026Review
- Enteric nervous system in exercise physiology: a microbiota-neural interface.npj metabolic health and disease · 2026Review
- Enteric glia, neuropeptides, and Parkinson's: impacts of calcitonin gene-related peptide on gut alpha synuclein.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Enteric nervous system and inflammatory bowel disease.Gastroenterology report · 2026Review
- Enteric nervous system in microbiota-associated gut inflammation.Frontiers in immunology · 2026Review
- MAIT Cells Maintain Intestinal Homeostasis Through IL-22 in an Experimental Colitis.Journal of inflammation research · 2026Article
- Enteric glial cells as regulators of the gut-brain axis: hormonal signaling, stress responses and progenitor potential.Frontiers in neuroscience · 2026Review
- FUT2-mediated intestinal fucosylation: a master regulator of host-microbiota symbiosis in health and disease.Frontiers in microbiology · 2026Review
- Gene Therapy in Crohn's Disease: Current Preclinical Challenges and Future Translational Avenues.Biomedicines · 2025Review
- CD44 is a macrophage receptor for TcdB fromGut microbes · 2025Article
- Neuroepithelial VIP-VIPR1 interactions differentially control enteric type 1 and type 2 immunity.Nature immunology · 2025Article
- Disease-specific alterations of the enteric nervous system in precancerous colonic mucosa and their implications for mucin regulation.Scientific reports · 2025Article
- The interaction network between group 3 innate lymphoid cells and other cells.Fundamental research · 2025Review
- The role of reactive enteric glia-macrophage interactions in acute and chronic inflammation.Neurogastroenterology and motility · 2025Review
- Bidirectional regulation of the brain-gut-microbiota axis following traumatic brain injury.Neural regeneration research · 2025Article
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
153 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Group 3 innate lymphoid cells (ILC3) are major regulators of inflammation and infection at mucosal barriers. ILC3 development is thought to be programmed, but how ILC3 perceive, integrate and respond to local environmental signals remains unclear. Here we show that ILC3 in mice sense their environment and control gut defence as part of a glial–ILC3–epithelial cell unit orchestrated by neurotrophic factors. We found that enteric ILC3 express the neuroregulatory receptor RET. ILC3-autonomous Ret ablation led to decreased innate interleukin-22 (IL-22), impaired epithelial reactivity, dysbiosis and increased susceptibility to bowel inflammation and infection. Neurotrophic factors directly controlled innate Il22 downstream of the p38 MAPK/ERK-AKT cascade and STAT3 activation. Notably, ILC3 were adjacent to neurotrophic-factor-expressing glial cells that exhibited stellate-shaped projections into ILC3 aggregates. Glial cells sensed microenvironmental cues in a MYD88-dependent manner to control neurotrophic factors and innate IL-22. Accordingly, glial-intrinsic Myd88 deletion led to impaired production of ILC3-derived IL-22 and a pronounced propensity towards gut inflammation and infection. Our work sheds light on a novel multi-tissue defence unit, revealing that glial cells are central hubs of neuron and innate immune regulation by neurotrophic factor signals.
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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.