ArticleNature microbiology2022
Group 3 innate lymphoid cell pyroptosis represents a host defence mechanism against Salmonella infection.
Article in Nature microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Engineering Salmonella as an immune-metabolic modulator of the tumor microenvironment.Trends in biotechnology · 2026Review
- LINGO4 coordinates ILC3-intrinsic IL-22 production and microbiota-mediated ILC3 homeostasis.The Journal of experimental medicine · 2026Article
- Current Applications and Immunological Considerations ofMicroorganisms · 2026Review
- Dendritic Cells and Their Crucial Role in Modulating Innate Lymphoid Cells for Treating and Preventing Infectious Diseases.Pathogens (Basel, Switzerland) · 2025Review
- Pyroptosis, a double-edged sword during pathogen infection: a review.Cell death discovery · 2025Review
- Regulation of innate lymphoid cell by microbial metabolites.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Mechanisms conferring multi-layered protection against intestinal Salmonella Typhimurium infection.FEMS microbiology reviews · 2025Review
- Interaction between Group 3 Innate Lymphoid Cells, Microbiota, and Intestinal Diseases: Mechanisms and Therapeutic Potential.Journal of innate immunity · 2025Review
- Deciphering the Role of Innate Lymphoid Cells Group 3 in the Gut Microenvironment: A Narrative Review of Their Novel Contributions to Autoimmune Disease Pathogenesis.Journal of inflammation research · 2025Review
- RIPK3 and caspase-8 interpret cytokine signals to regulate ILC3 survival in the gut.Mucosal immunology · 2024Article
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- Review
- 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
- A host-directed oxadiazole compound potentiates antituberculosis treatment via zinc poisoning in human macrophages and in a mouse model of infection.PLoS biology · 2024Article
- To die or not to die: Gasdermins in intestinal health and disease.Seminars in immunology · 2024Review
- Immunomodulatory biomaterials against bacterial infections: Progress, challenges, and future perspectives.Innovation (Cambridge (Mass.)) · 2023Review
- Nutrition impact on ILC3 maintenance and function centers on a cell-intrinsic CD71-iron axis.Nature immunology · 2023Article
- Review
- The thin line between conventional dendritic cells (cDCs) and group 3 innate lymphoid cells (ILC3s) in the gut.International immunology · 2023Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Group 3 innate lymphoid cells (ILC3s) produce interleukin (IL)-22 and coordinate with other cells in the gut to mount productive host immunity against bacterial infection. However, the role of ILC3s in Salmonella enterica serovar Typhimurium (S. Typhimurium) infection, which causes foodborne enteritis in humans, remains elusive. Here we show that S. Typhimurium exploits ILC3-produced IL-22 to promote its infection in mice. Specifically, S. Typhimurium secretes flagellin through activation of the TLR5-MyD88-IL-23 signalling pathway in antigen presenting cells (APCs) to selectively enhance IL-22 production by ILC3s, but not T cells. Deletion of ILC3s but not T cells in mice leads to better control of S. Typhimurium infection. We also show that S. Typhimurium can directly invade ILC3s and cause caspase-1-mediated ILC3 pyroptosis independently of flagellin. Genetic ablation of Casp1 in mice leads to increased ILC3 survival and IL-22 production, and enhanced S. Typhimurium infection. Collectively, our data suggest a key host defence mechanism against S. Typhimurium infection via induction of ILC3 death to limit intracellular bacteria and reduce IL-22 production.
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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.