ArticleThe Journal of experimental medicine2020
Noncanonical STAT3 activity sustains pathogenic Th17 proliferation and cytokine response to antigen.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Obefazimod in patients with moderate-to-severely active ulcerative colitis: efficacy and safety analysis from the 96-week open-label maintenance phase 2b study.Journal of Crohn's & colitis · 2025Trial
- Congenital iRHOM2 deficiency causes ADAM17 dysfunction and environmentally directed immunodysregulatory disease.Nature immunology · 2022Trial
- Regulation of follicular helper T cell subset differentiation in health and disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Myeloid-Derived Suppressor Cells in Inflammatory Arthritis.International journal of molecular sciences · 2026Review
- Dehydrocorydaline treatment suppresses Th17 differentiation via the mTOR-mediated STAT3-RORγt signaling in systemic lupus erythematosus.Molecular medicine (Cambridge, Mass.) · 2026Article
- Immunoprofiling Reveals GATA3 as a Prognostic Marker in Transformed Mycosis Fungoides.The Journal of dermatology · 2026Article
- Immunomodulatory and anti-inflammatory potential of S-nitrosoglutathione (GSNO) in multiple sclerosis: a review of mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- IL-15 Promotes Inflammatory Th17 Cells in the Intestine.Inflammatory bowel diseases · 2025Article
- mtSTAT3 suppresses rheumatoid arthritis by regulating Th17 and synovial fibroblast inflammatory cell death with IL-17-mediated autophagy dysfunction.Experimental & molecular medicine · 2025Article
- Unveiling the influence of tumor and immune signatures on immune checkpoint therapy in advanced lung cancer.eLife · 2024Article
- Ulcerative colitis: molecular insights and intervention therapy.Molecular biomedicine · 2024Review
- Aerobic physical training reduces severe asthma phenotype involving kinins pathway.Molecular biology reports · 2024Article
- Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024Review
- PIM kinases regulate early human Th17 cell differentiation.Cell reports · 2023Article
- Alpha-tocopherylquinone-mediated activation of the Aryl Hydrocarbon Receptor regulates the production of inflammation-inducing cytokines and ameliorates intestinal inflammation.Mucosal immunology · 2023Article
- CTRP4/interleukin-6 receptor signaling ameliorates autoimmune encephalomyelitis by suppressing Th17 cell differentiation.The Journal of clinical investigation · 2023Article
- Thymosin β4 Alleviates Autoimmune Dacryoadenitis via Suppressing Th17 Cell Response.Investigative ophthalmology & visual science · 2023Article
- SENP2 restrains the generation of pathogenic Th17 cells in mouse models of colitis.Communications biology · 2023Article
- Intrinsic STAT4 Expression Controls Effector CD4 T Cell Migration and Th17 Pathogenicity.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- CD47 haltsScience advances · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The STAT3 signaling pathway is required for early Th17 cell development, and therapies targeting this pathway are used for autoimmune disease. However, the role of STAT3 in maintaining inflammatory effector Th17 cell function has been unexplored. Th17ΔSTAT3 mice, which delete STAT3 in effector Th17 cells, were resistant to experimental autoimmune encephalomyelitis (EAE), a murine model of MS. Th17 cell numbers declined after STAT3 deletion, corresponding to reduced cell cycle. Th17ΔSTAT3 cells had increased IL-6-mediated phosphorylation of STAT1, known to have antiproliferative functions. Th17ΔSTAT3 cells also had reduced mitochondrial membrane potential, which can regulate intracellular Ca2+. Accordingly, Th17ΔSTAT3 cells had reduced production of proinflammatory cytokines when stimulated with myelin antigen but normal production of cytokines when TCR-induced Ca2+ flux was bypassed with ionomycin. Thus, early transcriptional roles of STAT3 in developing Th17 cells are later complimented by noncanonical STAT3 functions that sustain pathogenic Th17 cell proliferation and cytokine production.
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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.