ArticleProceedings of the National Academy of Sciences of the United States of America2010
Th17 plasticity in human autoimmune arthritis is driven by the inflammatory environment.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers.
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Who cites it
233 citing papers in PubMed, 437 citations in OpenAlex.
- IL-1β promotes the differentiation of polyfunctional human CCR6+CXCR3+ Th1/17 cells that are specific for pathogenic and commensal microbes.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Synovial Fluid Immune Cell Landscape in Juvenile Idiopathic Arthritis.European journal of immunology · 2026Article
- HLA-DRRespiratory research · 2026Article
- Identification and validation of KLRB1-related biomarkers in rheumatoid arthritis.Scientific reports · 2026Article
- Abnormal Pro-inflammatory Immune Cell Responses Precede Clinical Onset of Hypertensive Disorders of Pregnancy.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Transcriptional landscape of CD4+ T cells in Systemic Sclerosis.bioRxiv : the preprint server for biology · 2026Article
- CCL20-CCR6 signaling alters the metabolic reprogramming to promote the pathogenic Th17 cell differentiation.iScience · 2026Article
- IL-23 and monocyte interactions redirect human Th17.1 cells to an IL-17AFrontiers in immunology · 2026Article
- Second-order regulation: IFN-γ suppresses IL-17A-mediated type 3 inflammation.Frontiers in immunology · 2026Article
- Novel insights into the biology of childhood arthritis- lessons learned from the synovium.Arthritis research & therapy · 2025Review
- The interplay between M2-like macrophages and Th17.1 cells promotes the progression of early-stage sarcoidosis.Cell communication and signaling : CCS · 2025Article
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- Histone deacetylases facilitate Th17-cell differentiation and pathogenicity in autoimmune uveitis via CDK6/ID2 axis.Journal of advanced research · 2025Article
- Augmenting antitumor efficacy of Th17-derived Th1 cells through IFN-γ-induced type I interferon response network via IRF7.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Revisiting T Cells in Chronic Rhinosinusitis.Allergy, asthma & immunology research · 2024Review
- Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells.Cellular & molecular immunology · 2024Review
- Th17 cell function in cancers: immunosuppressive agents or anti-tumor allies?Cancer cell international · 2024Review
- A targetable type III immune response with increase of IL-17A expressing CD4Nature cancer · 2024Article
- Study of pathogenic T-helper cell subsets in Asian Indian patients with Takayasu arteritis.Immunologic research · 2024Article
- NRF2 is a spatiotemporal metabolic hub essential for the polyfunctionality of Th2 cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
173 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In several murine models of autoimmune arthritis, Th17 cells are the dominant initiators of inflammation. In human arthritis the majority of IL-17-secreting cells within the joint express a cytokine phenotype intermediate between Th17 and Th1. Here we show that Th17/1 cells from the joints of children with inflammatory arthritis express high levels of both Th17 and Th1 lineage-specific transcription factors, RORC2 and T-bet. Modeling the generation of Th17/1 in vitro, we show that Th17 cells "convert" to Th17/1 under conditions that mimic the disease site, namely low TGFbeta and high IL-12 levels, whereas Th1 cells cannot convert to Th17. Th17/1 cells from the inflamed joint share T-cell receptor (TCR) clonality with Th17 cells, suggesting a shared clonal origin between Th17 and Th17/1 cells in arthritis. Using CD161, a lectin-like receptor that is a marker of human Th17, we show synovial Th17 and Th17/1 cells, and unexpectedly, a large proportion of Th1 cells express CD161. We provide evidence to support a Th17 origin for Th1 cells expressing CD161. In vitro, Th17 cells that convert to a Th1 phenotype maintain CD161 expression. In the joint CD161+ Th1 cells share features with Th17 cells, with shared TCR clonality, expression of RORC2 and CCR6 and response to IL-23, although they are IL-17 negative. We propose that the Th17 phenotype may be unstable and that Th17 cells may convert to Th17/1 and Th1 cells in human arthritis. Therefore therapies targeting the induction of Th17 cells could also attenuate Th17/1 and Th1 effector populations within the inflamed joint.
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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.