HIV replication can be inhibited by CXCR5⁺CD8 T cells (follicular cytotoxic T cell [TFC]) which transfer into B‐cell follicles where latent HIV infection persists. However, how cytokines affect TFC remain unclear. Understanding which cytokines show the ability to affect TFC could be a key strategy toward curing HIV. Similar mechanisms could be used for the growth and transfer of TFCs and follicular helper T (TFH) cells; as a result, we hypothesized that cytokines IL‐6, IL‐21, and transforming growth factor‐β (TGF‐β), which are necessary for the differentiation of TFH cells, could also dictate the development of TFCs. In this work, lymph node mononuclear cells and peripheral blood mononuclear cells from HIV‐infected individuals were cocultured with IL‐6, IL‐21, and TGF‐β. We then carried out T‐cell receptor (TCR) repertoire analysis to compare the differences between CXCR5^– and CXCR5⁺CD8 T cells. Our results showed that the percentage and function of TFC can be enhanced by stimulation with TGF‐β. Besides, TGF‐β stimulation enhanced the diversity of TCR and complementarity‐determining region 3 sequences. HIV DNA showed a negative correlation with TFC. The use of TGF‐β to promote the expression of CXCR5⁺CD8 T cells could become a new treatment approach for curing HIV.

中文翻译：

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转化生长因子-β可促进HIV特异性CXCR5 + CD8 T细胞的功能。

HIV复制可被CXCR5 ⁺抑制CD8 T细胞（滤泡性细胞毒性T细胞[TFC]）会转移到B细胞滤泡中，在那里HIV潜伏的感染持续存在。但是，尚不清楚细胞因子如何影响TFC。了解哪些细胞因子具有影响TFC的能力可能是治愈HIV的关键策略。类似的机制可用于TFC和滤泡辅助性T（TFH）细胞的生长和转移。结果，我们假设，分化TFH细胞所必需的细胞因子IL-6，IL-21和转化生长因子β（TGF-β）也可能决定了TFC的发展。在这项工作中，将来自HIV感染者的淋巴结单核细胞和外周血单核细胞与IL-6，IL-21和TGF-β共培养。然后，我们进行了T细胞受体（TCR）谱表分析，以比较CXCR5之间的差异^–和CXCR5 ⁺ CD8 T细胞。我们的结果表明，TGF-β刺激可提高TFC的百分比和功能。此外，TGF-β刺激增强了TCR和互补决定区3序列的多样性。HIV DNA与TFC呈负相关。使用TGF-β促进CXCR5 ⁺ CD8 T细胞表达可能成为治愈HIV的新方法。