ArticleThe Journal of experimental medicine2015
Unique and redundant functions of NKp46+ ILC3s in models of intestinal inflammation.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 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
151 citing papers in PubMed, 208 citations in OpenAlex.
- Effect of the intestinal microbiota on TSeminars in immunopathology · 2026Review
- Cell type-specific enhancers regulate IL-22 expression in innate and adaptive type 3 lymphoid cells.Nature communications · 2026Article
- The development of innate lymphoid cells.Nature immunology · 2026Review
- Distinguishing Features of ILC2s During Type 2 Immune Responses.European journal of immunology · 2026Review
- tRNA mCell discovery · 2026Article
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- The aryl hydrocarbon receptor: a rehabilitated target for therapeutic immune modulation.Nature reviews. Drug discovery · 2025Review
- Elevated nitric oxide during colitis restrains GM-CSF production in ILC3 cells via suppressing an AhR-Cyp4f13-NF-κB axis.Nature communications · 2025Article
- Enteric tuft cell inflammasome activation drives NKp46+ILC3 IL22 via PGD2 and inhibits Salmonella.The Journal of experimental medicine · 2025Article
- Article
- Fiber- and acetate-mediated modulation of MHC-II expression on intestinal epithelium protects from Clostridioides difficile infection.Cell host & microbe · 2025Article
- NKp46 enhances type 1 innate lymphoid cell proliferation and function and anti-acute myeloid leukemia activity.Nature communications · 2025Article
- Tissue-resident immune cells: from defining characteristics to roles in diseases.Signal transduction and targeted therapy · 2025Review
- Interaction between Group 3 Innate Lymphoid Cells, Microbiota, and Intestinal Diseases: Mechanisms and Therapeutic Potential.Journal of innate immunity · 2025Review
- Advancements in the Study of the Immune Molecule NKp46 in Immune System-related Diseases.Clinical reviews in allergy & immunology · 2024Review
- NKp46Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Strategies for targeting cytokines in inflammatory bowel disease.Nature reviews. Immunology · 2024Review
- OLFM4 modulates intestinal inflammation by promoting IL-22Communications biology · 2024Article
- Group 3 innate lymphoid cells in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2024Review
91 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Group 3 ILCs (ILC3s) are innate sources of IL-22 and IL-17 and include lymphoid tissue-inducer (LTi)-like and NKp46(+) subsets. Both depend on RORγt and aryl hydrocarbon receptor, but NKp46(+)ILC3s also require Notch and T-bet for their development and are transcriptionally distinct. The extent to which these subsets have unique functions, especially in the context of T cell- and B cell-sufficient mice, remains largely unclear. To investigate the specific function of NKp46(+)ILC3s among other ILC3 subsets and T cells, we generated mice selectively lacking NKp46(+)ILC3s or all ILC3s and crossed them to T cell-deficient mice, thus maintaining B cells in all mice. In mice lacking T cells, NKp46(+)ILC3s were sufficient to promote inflammatory monocyte accumulation in the anti-CD40 innate colitis model through marked production of GM-CSF. In T cell-competent mice, lack of NKp46(+)ILCs had no impact on control of intestinal C. rodentium infection, whereas lack of all ILC3s partially impaired bacterial control. Thus, NKp46(+)ILC3s have a unique capacity to promote inflammation through GM-CSF-induced accumulation of inflammatory monocytes, but are superseded by LTi-like ILC3s and T cells in controlling intestinal bacterial infection.
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.