ArticleImmunity2021
The TGF-β superfamily cytokine Activin-A is induced during autoimmune neuroinflammation and drives pathogenic Th17 cell differentiation.
Article in Immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 114 citations in OpenAlex.
- SKI is critical to counter TGF-β signaling to promote T cell function and autoimmunity.Science advances · 2026Article
- A cell-intrinsic glucocorticoid biosynthesis and sensing circuit maintains a homeostatic Th17 cell state.Immunity · 2026Article
- Interleukin-6 Downregulates T Helper 17 Cytokines via Indoleamine 2,3-Dioxygenase 1 at the Maternal-Fetal Interface.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Artificial Intelligence-Driven Construction of Predictive and Druggable Frameworks to an In Silico Bioengineering Evidence Support for Therapy of Esophageal Squamous Cell Carcinoma Patients: Insights from a Toll-like Receptor Signal with Th17 and T Helper Microenvironment.Bioengineering (Basel, Switzerland) · 2026Article
- Contextualizing TNature reviews. Immunology · 2026Review
- ActIIR inhibition improves motor outcome and preserves muscle fibers after experimental autoimmune neuritis.Acta neuropathologica communications · 2026Article
- Endothelial C-type natriuretic peptide/guanylyl cyclase-B signaling prevents pulmonary arterial hypertension.Nature communications · 2026Article
- Role of solute carrier family 7 member 7 in cancer: opportunities for tumor microenvironment research.Journal for immunotherapy of cancer · 2026Review
- NMI promotes the secretion of IL-17 and exacerbates psoriasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- ALK5 inhibition reduces HDM-induced inflammation and oxidative injury by regulating KLF4-mediated glycolysis in BEAS-2B cells.Journal of bioenergetics and biomembranes · 2026Article
- Advances in immunological research on male infertility.Frontiers in reproductive health · 2026Review
- Integrated Multi-Omics Analyses Identify Acupuncture-Associated Changes in Gut Microbiota, Short-Chain Fatty Acids, and TNC Gene Expression in Chronic Migraine Rats.Journal of inflammation research · 2026Article
- Integrated single-cell TCR analysis across tissue identifies GZMKInternational journal of biological sciences · 2026Article
- Key role for inhibins in effective T cell activation, migration and Th17 differentiation.FEBS open bio · 2026Article
- Transcriptomics, lifestyle, and autoimmune thyroiditis: an integrated association study.Frontiers in immunology · 2026Article
- Targeting Gut Immune Dysregulation: Therapeutic Potential of Huangqin Decoction in Inflammatory Bowel Disease.Chinese journal of integrative medicine · 2025Review
- CircRNA-Based Therapeutics: a New Frontier in Neuroinflammation Treatment.Molecular neurobiology · 2025Review
- IL-15 Promotes Inflammatory Th17 Cells in the Intestine.Inflammatory bowel diseases · 2025Article
- Epithelial pyroptosis-induced TREM1Cell death discovery · 2025Article
- Fructose intake driven glycolysis-ROS-EGFR axis specifically promotes the generation and pathogenicity of Th17 cells.Nature communications · 2025Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Th17 cells are known to exert pathogenic and non-pathogenic functions. Although the cytokine transforming growth factor β1 (TGF-β1) is instrumental for Th17 cell differentiation, it is dispensable for generation of pathogenic Th17 cells. Here, we examined the T cell-intrinsic role of Activin-A, a TGF-β superfamily member closely related to TGF-β1, in pathogenic Th17 cell differentiation. Activin-A expression was increased in individuals with relapsing-remitting multiple sclerosis and in mice with experimental autoimmune encephalomyelitis. Stimulation with interleukin-6 and Activin-A induced a molecular program that mirrored that of pathogenic Th17 cells and was inhibited by blocking Activin-A signaling. Genetic disruption of Activin-A and its receptor ALK4 in T cells impaired pathogenic Th17 cell differentiation in vitro and in vivo. Mechanistically, extracellular-signal-regulated kinase (ERK) phosphorylation, which was essential for pathogenic Th17 cell differentiation, was suppressed by TGF-β1-ALK5 but not Activin-A-ALK4 signaling. Thus, Activin-A drives pathogenic Th17 cell differentiation, implicating the Activin-A-ALK4-ERK axis as a therapeutic target for Th17 cell-related diseases.
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