ArticleArthritis research & therapy2025
Modulating IL-21-driven B cell responses in idiopathic inflammatory myopathies via inhibition of the JAK/STAT pathway.
Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Rhabdomyolysis in a patient with lung cancer with sintilimab-induced overlap syndrome and hypothyroidism: A case report.Experimental and therapeutic medicine · 2026Article
- Aberrant IL-21/STAT3 signaling disrupts regulatory T cell function and CD4Frontiers in immunology · 2026Article
- Targeted Therapy for Idiopathic Inflammatory Myopathy.Journal of cachexia, sarcopenia and muscle · 2025Review
- Challenges and strategies in clinical applications of CAR-T therapy for autoimmune diseases.Journal of hematology & oncology · 2025Review
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11 authors.
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Abstract
backgroundIdiopathic inflammatory myopathies (IIM) are autoimmune disorders characterized by muscle inflammation and autoreactive B cell responses. The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway is essential for B cell functions, making it a promising therapeutic target. This study explores the potential of tofacitinib, a JAK1/JAK3 inhibitor, to modulate B cell activity in IIM.
methodsPeripheral B cell populations from dermatomyositis (DM), anti-synthetase syndrome (ASyS) and overlap myositis (OM) patients were analyzed by flow cytometry. Peripheral blood mononuclear cells (PBMC) or sorted memory B cells were cultured with tofacitinib and stimulated with combinations of CD40, IL-21, IL-2, BAFF and CpG. B cell proliferation, differentiation and (auto)antibody, cytokine/chemokine production were assessed by flow cytometry, Luminex, and ELISA/ELiA assays.
resultsThe IIM peripheral B cell compartment had elevated transitional and naive B cells, with reduced Bmem frequencies compared to healthy donors. Tofacitinib significantly inhibited CD40/IL-21-induced B cell proliferation, plasmablast formation and function in PBMC and B cell-only cultures across all IIM subgroups, predominantly affecting the IL-21-induced differentiation and antibody production. Remarkably, tofacitinib reduced the levels of anti-Jo1 autoantibodies, as well as of CXCL10 and CXCL13 in ASyS memory B cell cultures.
conclusionsThese findings highlight the B cell involvement in IIM, evidenced by altered peripheral B cell composition in active disease and the effective inhibition of essential B cell responses, including proliferation, differentiation, and (auto)antibody production, by tofacitinib in vitro. This positions the JAK/STAT pathway as a promising new therapeutic target to modulate B cell activity in IIM.
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