Type 1 helper T cells generate CXCL9/10-producing T-bet+ effector B cells potentially involved in the pathogenesis of rheumatoid arthritis

Efficacy of B-cell depletion therapy highlights the antibody-independent effector functions B cells in rheumatoid arthritis (RA). Given type 1 helper T (Th1) abundant synovial fluid (SF) RA, we have determined whether Th1 could generate novel cells. Microarray and qPCR analysis identified CXCL9/10 transcripts as highly expressed genes upon BCR/CD40/IFN-? stimulation. Activated promoted generation CXCL9/10-producing T-bet+ Expression was most pronounced CXCR3+ switched memory Compared with peripheral blood, SFRA enriched activated that coexisted Intriguingly, anti-IFN-? antibody JAK inhibitors significantly abrogated cell derived facilitated migration CD4+ These findings suggest be an ideal pathogenic target for RA therapy.