ArticleImmunity2018
Autoimmune Th17 Cells Induced Synovial Stromal and Innate Lymphoid Cell Secretion of the Cytokine GM-CSF to Initiate and Augment Autoimmune Arthritis.
Article in Immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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
108 citing papers in PubMed, 178 citations in OpenAlex.
- Immune cell-derived membrane nanovesicles: A promethean fire for autoimmune disease therapy through immune cell mimicry.Bioactive materials · 2026Review
- ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.Clinical and translational medicine · 2026Article
- Engineering autoimmune disease models using organoids: Harnessing microenvironmental engineering for precision medicine and immunological recapitulation.Bioengineering & translational medicine · 2026Review
- Innate lymphoid cells in rheumatoid arthritis as mediators of pathology and resolution.Nature reviews. Rheumatology · 2026Review
- Tissue-restricted secondary TCR engagement drives the transition from stem-like to CD200Nature immunology · 2026Article
- Pathogenic GM-CSF drives functional diversification of inflammatory macrophages in autoimmune arthritis.Science advances · 2026Article
- Inhibition of IL-6/STAT3 Signaling by N-Trans-Hibiscusamide and Its Derivative in a Mouse Model of Collagen-Induced Arthritis.Food science & nutrition · 2026Article
- Two new mycobactins, mycobactins U and V, and their ferric complexes isolated from Mycolicibacterium septicum IFM 12283.Journal of natural medicines · 2026Article
- The Gut Microbiota: Emerging Evidence in Autoimmune and Inflammatory Diseases.Research (Washington, D.C.) · 2026Review
- AIM2 as an Immunogenic Cell Death (ICD)-related hub gene in rheumatoid arthritis: identification and functional validation.Clinical rheumatology · 2025Article
- Tissue-Resident Memory T Cells in Rheumatoid Immune Diseases: Pathogenic Mechanisms and Therapeutic Strategies.Biomedicines · 2025Review
- Targeting GM-CSF in Rheumatoid Arthritis: Advances in Cytokine-Directed Immunotherapy and Clinical Implications.Life (Basel, Switzerland) · 2025Review
- TScience immunology · 2025Article
- Cross-Sectional and Longitudinal Immunoprofiling of Oligoarticular Juvenile Idiopathic Arthritis Reveals Different Patterns in Synovial Fluid and Plasma.Scandinavian journal of immunology · 2025Article
- Osteoimmunology: Crosstalk Between T Cells and Osteoclasts in Osteoporosis.Clinical reviews in allergy & immunology · 2025Review
- Synovial Fluid as a Crucial Component of the Joint Microenvironment in Rheumatoid Arthritis.Immune network · 2025Review
- ER O-glycosylation in synovial fibroblasts drives cartilage degradation.Nature communications · 2025Article
- Id2 exacerbates the development of rheumatoid arthritis by increasing IFN-γ production in CD4Clinical and translational medicine · 2025Article
- Migration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines.Nature communications · 2025Article
- Immunological Regulation of Fibrosis During Heart Failure: It Takes Two to Tango.Biomolecules · 2025Review
48 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Despite the importance of Th17 cells in autoimmune diseases, it remains unclear how they control other inflammatory cells in autoimmune tissue damage. Using a model of spontaneous autoimmune arthritis, we showed that arthritogenic Th17 cells stimulated fibroblast-like synoviocytes via interleukin-17 (IL-17) to secrete the cytokine GM-CSF and also expanded synovial-resident innate lymphoid cells (ILCs) in inflamed joints. Activated synovial ILCs, which expressed CD25, IL-33Ra, and TLR9, produced abundant GM-CSF upon stimulation by IL-2, IL-33, or CpG DNA. Loss of GM-CSF production by either ILCs or radio-resistant stromal cells prevented Th17 cell-mediated arthritis. GM-CSF production by Th17 cells augmented chronic inflammation but was dispensable for the initiation of arthritis. We showed that GM-CSF-producing ILCs were present in inflamed joints of rheumatoid arthritis patients. Thus, a cellular cascade of autoimmune Th17 cells, ILCs, and stromal cells, via IL-17 and GM-CSF, mediates chronic joint inflammation and can be a target for therapeutic intervention.
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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.