The conditions leading to the activation/differentiation of T-helper (Th) cells dedicated for B-cell antibody production are still poorly characterized. We now demonstrate that interleukin-6 (IL-6) promotes the differentiation of naive T lymphocytes into helper cells able to promote B-cell activation and antibody secretion. IL-6-driven acquisition of B-cell help capacity requires expression of the signal transducer and activator of transcription 3 (STAT3), but not STAT4 or STAT6 transcription factors, suggesting that the ability to provide help to B cells is not restricted to a well-defined Th1 or Th2 effector population. T cell-specific STAT3-deficient mice displayed reduced humoral responses in vivo that could not be related to an altered expansion of CXCR5-expressing helper T cells. IL-6 was shown to promote IL-21 secretion, a cytokine that was similarly found to promote the differentiation of naive T cells into potent B-cell helper cells. Collectively, these data indicate that the ability to provide B-cell help is regulated by IL-6/IL-21 through STAT3 activation, independently of Th1, Th2, Th17, or follicular helper T cell (T(FH)) differentiation.

中文翻译：

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Interleukin-6/STAT3 信号调节初始 T 细胞获得 B 细胞辅助能力的能力

导致专用于 B 细胞抗体生产的 T 辅助 (Th) 细胞活化/分化的条件仍然很差。我们现在证明白细胞介素 6 (IL-6) 促进幼稚 T 淋巴细胞分化为能够促进 B 细胞活化和抗体分泌的辅助细胞。IL-6 驱动的 B 细胞辅助能力的获得需要信号转导和转录激活因子 3 (STAT3) 的表达，而不是 STAT4 或 STAT6 转录因子的表达，这表明为 B 细胞提供帮助的能力不仅限于明确定义的 Th1 或 Th2 效应子群体。T 细胞特异性 STAT3 缺陷小鼠在体内表现出减少的体液反应，这与表达 CXCR5 的辅助 T 细胞的扩增改变无关。IL-6 显示促进 IL-21 分泌，一种细胞因子，同样被发现可促进幼稚 T 细胞分化为有效的 B 细胞辅助细胞。总的来说，这些数据表明提供 B 细胞帮助的能力由 IL-6/IL-21 通过 STAT3 激活调节，独立于 Th1、Th2、Th17 或滤泡辅助 T 细胞 (T(FH)) 分化。