{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu B"],"funding":["National Institute of Environmental Health Sciences","National Institute of Allergy and Infectious Diseases","National Multiple Sclerosis Society","NIAID NIH HHS"],"pagination":["308-323.e6"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7878438"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["54(2)"],"pubmed_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 Th"],"journal":["Immunity"],"pubmed_title":["The TGF-β superfamily cytokine Activin-A is induced during autoimmune neuroinflammation and drives pathogenic Th17 cell differentiation."],"pmcid":["PMC7878438"],"funding_grant_id":["R01 AI123193","R01 AI131238","R01 AI160774"],"pubmed_authors":["Zhou M","Wan YY","Guo Z","Markovic-Plese S","Wu B","Li P","Li JL","Zhang S","Xu X","Seyedsadr M","Bi Y"],"additional_accession":[]},"is_claimable":false,"name":"The TGF-β superfamily cytokine Activin-A is induced during autoimmune neuroinflammation and drives pathogenic Th17 cell differentiation.","description":"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 Th","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Feb","modification":"2026-04-14T19:12:28.451Z","creation":"2025-04-06T14:57:10.551Z"},"accession":"S-EPMC7878438","cross_references":{"pubmed":["33421362"],"doi":["10.1016/j.immuni.2020.12.010"]}}