Interleukin-6/STAT3 signaling regulates the ability of naive T cells to acquire B-cell help capacities
Interleukin-6/STAT3 signaling regulates the ability of naive T cells to acquire B-cell help capacities
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DOI：
10.1182/blood-2008-04-154682
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发表时间：
2009-03-12
期刊：
影响因子：
20.3
通讯作者：
Andris, Fabienne
中科院分区：
文献类型：
--
作者：
Eddahri, Fouad;Denanglaire, Sebastien;Andris, Fabienne
导致专用于B细胞抗体产生的辅助性T细胞（Th）的活化/分化的条件仍然缺乏表征。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子和转录激活子3（STAT 3）的表达，但不需要STAT 4或STAT 6转录因子的表达，这表明向B细胞提供辅助的能力不限于明确定义的Th 1或Th 2效应子群体。T细胞特异性STAT 3缺陷小鼠显示体内体液应答降低，这与表达CXCR 5的辅助T细胞的扩增改变无关。IL-6显示促进IL-21分泌，IL-21是一种类似地发现促进幼稚T细胞分化为有效B细胞辅助细胞的细胞因子。总的来说，这些数据表明，提供B细胞帮助的能力是由IL-6/IL-21通过STAT 3激活，独立于Th 1，Th 2，Th 17，或滤泡辅助T细胞（T-FH）分化。（血。2009;113：2426-2433）
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. (Blood. 2009;113:2426-2433)