T cell dysfunction is a common characteristic in leukemia patients that significantly impacts clinical treatment and prognosis. However, the mechanism underlying T cell dysfunction and its reversal remains unclear. In this study, in accordance with our previous findings, we found that the expression of NFAT2 and pri-miR-17 ~ 92 are lower in peripheral blood CD3⁺ T cells from chronic myelogenous leukemia (CML) patients by gene expression analysis. We further demonstrate that the NFAT2-induced activation, differentiation, and expression of cytokines in human umbilical cord blood CD8⁺ naïve T cells are miR-20a-5p dependent. We also preliminarily explored the relationship between NFAT2 and miR-20a-5p in naive T cells. These results suggest that NFAT2 and miR-20a are crucial for regulating functional CD8⁺ T cells. Additionally, their alteration may be related to CD8⁺ T cell dysfunction in CML patients; thus, NFAT2 and miR-20a-5p may be considered potential targets for revising T cell function in leukemia immunotherapy.

T细胞功能障碍是白血病患者的共同特征，显着影响临床治疗和预后。然而，T细胞功能障碍及其逆转的机制仍不清楚。在本研究中，根据我们之前的研究结果，我们通过基因表达分析发现慢性粒细胞白血病（CML）患者外周血CD3 ^{+ T细胞中NFAT2和pri-miR-17~92的表达较低。}我们进一步证明了 NFAT2 诱导的人脐带血 CD8 ^{+细胞因子的激活、分化和表达}初始 T 细胞依赖于 miR-20a-5p。我们还初步探讨了 NFAT2 与 miR-20a-5p 在幼稚 T 细胞中的关系。这些结果表明 NFAT2 和 miR-20a 对于调节功能性 CD8 ⁺ T 细胞至关重要。此外，它们的改变可能与CML 患者的 CD8 ^{+ T 细胞功能障碍有关。}因此，NFAT2 和 miR-20a-5p 可能被认为是在白血病免疫治疗中修改 T 细胞功能的潜在靶点。