Modulating IL-21-driven B cell responses in idiopathic inflammatory myopathies via inhibition of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway
Authors' conclusion
These 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.
Study context
- Population
- Patients with idiopathic inflammatory myopathies (IIM) (dermatomyositis (DM), anti-synthetase syndrome (ASyS), overlap myositis); Peripheral blood mononuclear cells (PBMC) or sorted memory B cells cultured with tofacitinib and stimulated with CD40, IL-21, IL-2, BAFF and CpG
- Comparison
- Tofacitinib vs no tofacitinib in stimulated PBMC or sorted memory B cell cultures; IIM patients vs healthy donors (peripheral B cell populations)
Methodological detailsin vitro, flow cytometry, Luminex, ELISA/ELiA assays
- In vitro
- Flow cytometry
- Luminex
- ELISA/ELiA assays
Main finding
As reported in the abstract
- IIM peripheral B cell compartment: elevated transitional and naive B cells, reduced Bmem frequencies vs 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 IL-21-induced differentiation and antibody production
- Tofacitinib reduced anti-Jo1 autoantibodies, CXCL10 and CXCL13 in ASyS memory B cell cultures
- In vitro
Original publication
Modulating IL-21-driven B cell responses in idiopathic inflammatory myopathies via inhibition of the JAK/STAT pathway. Arthritis Res Ther. Published 1 April 2025. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →