期刊
JOURNAL OF IMMUNOLOGY
卷 194, 期 6, 页码 2482-2485出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401190
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资金
- Arthritis Research UK
- University College London Hospital Comprehensive Biomedical Research Centre
- Versus Arthritis [18882] Funding Source: researchfish
B cells require CD4(+) T follicular helper (Tfh) cells to progress through the germinal center and provide protective Ab responses. In this article, we reveal a reciprocal interaction whereby circulating human plasmablasts are potent inducers of the Tfh cell-differentiation program, including the expression of their key transcription factor Bcl-6. The markedly increased propensity of plasmablasts, compared with naive B cells, to induce Tfh cell differentiation was due to their increased production of IL-6. Specific targeting of IL-6 using tocilizumab therapy in patients with rheumatoid arthritis led to a significant reduction in circulating Tfh cell numbers and IL-21 production, which was correlated with reduced plasmablast formation. Our data uncover a positive-feedback loop between circulating plasmablasts and Tfh cells that could sustain autoimmunity and spread Ab-driven inflammation to unaffected sites; this represents an important therapeutic target, as well as reveals a novel mechanism of action for tocilizumab.
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