本研究旨在调查活动性结核患者免疫细胞亚群及T细胞免疫分子的表达水平，了解活动性结核患者的细胞免疫特征。通过纳入2020年12月—2021年5月活动性结核患者(active tuberculosis，ATB)21例以及健康对照(healthy controls, HC)10例，采集受试者的外周血，进行全血细胞表面和细胞内流式染色，以评估外周血T细胞亚群的比例及功能状态。采用Fisher确切概率法比较计数资料，采用非参数Mann-Whitney U检验比较连续变量。结果显示，ATB患者CD4^＋ T细胞中滤泡辅助性T细胞(follicular helper T cell, Tfh)显著低于HC组，CD8^＋ T细胞中初始T细胞、耗竭前体T细胞显著减少(P<0.05)，而终末耗竭T细胞显著高于HC组(P<0.05)。ATB组CD4^＋ T细胞表面CD62L表达显著降低(P＝0.01)，CD8^＋ T细胞表面TIM-3、CD127及胞内T-bet、TCF1的表达水平显著低于HC组(P<0.05)，而KLRG1、PD1、TIGIT 以及CD69 显著高于HC组(P<0.05)。本实验证实，活动性结核感染患者T细胞表现出独特的免疫表型，其促炎能力下降而抗炎能力增强，同时CD8^＋ T细胞向耗竭表型分化加剧。

In order to understand the T cell immune status of active tuberculosis (ATB) patients, the study compared the expression levels of T cell immune molecules and the proportion of T cell functional subsets between ATB patients and healthy controls (HC). A total of 21 ATB patients and 10 HC were enrolled from December 2020 to May 2021. Peripheral blood samples were collected from the participants, and flow cytometry was performed for surface and intracellular staining to investigate the proportion and functional status of peripheral blood T cells. Fisher’s exact probability test and non-parametric Mann-Whitney U test were used to analyze the data. The result showed that the proportion of Tfh in CD4^＋ T cells was significantly lower in ATB patients than that in HC group (P<0.05), and the proportions of naive T cells, progenitor exhausted T cells in CD8^＋ T cells were lower in ATB patients compared to HC, while terminal exhausted T cells were higher (P<0.05). The expression of CD62L on CD4^＋ T cells was significantly lower in the ATB group (P＝0.01). The expression of TIM-3 and CD127 on CD8^＋ T cells as well as T-bet and TCF1 in CD8^＋ T cells in the ATB group were also significantly lower than those in the HC group, while KLRG1, PD1, TIGIT, and CD69 were higher (P<0.05). In conclusion, T cells from active tuberculosis patients exhibit a unique immune phenotype characterized by reduced pro-inflammatory capacity and increased anti-inflammatory capacity, meanwhile exacerbated differentiation towards an exhausted phenotype in CD8^＋ T cells.