ArticleNature medicine2017
Resolution of inflammation by interleukin-9-producing type 2 innate lymphoid cells.
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Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.
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168citing papers in PubMed
13.4field-weighted citation impact, top 1% of its field
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Who cites it
168 citing papers in PubMed, 285 citations in OpenAlex.
- Interleukin-9 Facilitates Osteoclastogenesis in Rheumatoid Arthritis.International journal of molecular sciences · 2021Trial
- IL-9 Is Essential for ILC2-Mediated but Not Th2- and Th17-Cell-Mediated Allergic Airway Inflammation in Mice.European journal of immunology · 2026Article
- Increased group 2 Innate lymphoid cell (ILC2) activity in pediatric familial mediterranean fever patients with spondyloarthropathy.Clinical and experimental medicine · 2026Article
- An early protective effect of IL-9 in murine systemic lupus erythematosus.ImmunoHorizons · 2026Article
- Innate lymphoid cells in rheumatoid arthritis as mediators of pathology and resolution.Nature reviews. Rheumatology · 2026Review
- Th9 cells at the intersection of IBD and colorectal cancer: a context-dependent factor in carcinogenesis.Inflammation and regeneration · 2026Review
- Article
- ILC2-derived IL-9 activates regulatory T cells to facilitate post-myocardial infarction repair.Cell communication and signaling : CCS · 2026Article
- Mechanisms of osteoclast activation in inflammatory bone loss in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Resolution Pharmacology: State-of-the-art and therapeutic landscape.Pharmacological reviews · 2025Review
- The role of the IL-9‒NLRP3 axis in insulin resistance and adipose tissue inflammation during diet-induced obesity.Cellular & molecular immunology · 2025Article
- Th Cell Phenotypes and Their Correlations with Disease Activity in Patients with Rheumatoid Arthritis.Journal of clinical medicine · 2025Article
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Plasma proteome analysis of rheumatic patients reveals differences in fingerprints based on cardiovascular history: a pilot study.Proteome science · 2025Article
- Association of 41 Inflammatory Cytokines With Common Oral Diseases.International dental journal · 2025Article
- Metabolic regulation of Th9 cell differentiation: insights for IL-9-driven diseases.Frontiers in immunology · 2025Review
- Chemokines in the resolution of inflammation: key players and targets for therapeutic modulation.Frontiers in immunology · 2025Review
- Innate lymphoid cells in the spotlight: from biomarkers to blueprint for innovative immunotherapy.Frontiers in immunology · 2025Review
- Multi-organ pathology in a small porcine model of cytokine storm syndrome characteristics.Frontiers in immunology · 2025Article
- Biological mechanisms of pulmonary inflammation and its association with seropositive rheumatoid arthritis.Frontiers in immunology · 2025Review
108 more citing papers are in PubMed but not listed here.
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Authors and funding
25 authors at 8 institutions in 6 countries.
Simon RauberDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Markus LuberDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Stefanie WeberDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Lisa MaulDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Alina SoareDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Thomas WohlfahrtDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Neng-Yu LinDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Katharina DietelDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Aline BozecDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Martin HerrmannDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0002-0258-2484
Mark H KaplanHerman B Wells Center for Pediatric Research, Indianapolis, Indiana, USA.ORCID http://orcid.org/0000-0002-2923-8245
Benno WeigmannDepartment of Internal Medicine 1, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Mario M ZaissDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Ursula FearonMolecular Rheumatology, School of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Douglas J VealeCentre for Arthritis and Rheumatic Diseases, St. Vincent's University Hospital, Dublin, Ireland.
Juan D CañeteDepartamento de Reumatología, Hospital Clínic de Barcelona e IDIBAPS, Barcelona, Spain.
Oliver DistlerDivision of Rheumatology, University Hospital Zurich, Zurich, Switzerland.
Felice RivelleseCentre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London and Barts Health NHS Trust, London, UK.
Costantino PitzalisCentre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London and Barts Health NHS Trust, London, UK.
Markus F NeurathDepartment of Internal Medicine 1, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Andrew N J McKenzieMRC Laboratory of Molecular Biology, Cambridge, UK.
Stefan WirtzDepartment of Internal Medicine 1, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Georg SchettDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Jörg H W DistlerDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Andreas RammingDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEQueen Mary University of London · GBHospital Clínic de Barcelona · ESIndiana University – Purdue University Indianapolis · USMRC Laboratory of Molecular Biology · GBSt. Vincent's University Hospital · IETrinity College Dublin · IEUniversity Hospital of Zurich · CH
Funding
The role of PU.1 in T helper cell heterogeneityR01AI057459 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 2005 to 2025
$8.2MTh9 cells in immediate hypersensitivityR01AI129241 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPLAN, MARK H · 2017 to 2021
$2.0MMedical Research Council G0800648Medical Research Council MC_U105178805NIAID NIH HHS R01 AI057459NIAID NIH HHS R01 AI129241Wellcome Trust
Abstract
Inflammatory diseases such as arthritis are chronic conditions that fail to resolve spontaneously. While the cytokine and cellular pathways triggering arthritis are well defined, those responsible for the resolution of inflammation are incompletely characterized. Here we identified interleukin (IL)-9-producing type 2 innate lymphoid cells (ILC2s) as the mediators of a molecular and cellular pathway that orchestrates the resolution of chronic inflammation. In mice, the absence of IL-9 impaired ILC2 proliferation and activation of regulatory T (T
Indexed as
AdultAgedAnimalsArthritis, ExperimentalArthritis, RheumatoidCell ProliferationDisease Models, AnimalFemaleFlow CytometryGene Expression ProfilingGene Transfer TechniquesHumansImmunity, InnateInflammationInterleukin-9In Vitro TechniquesInterleukin-9
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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.