Patients affected by pulmonary tuberculosis (PTB) manifest deficiencies in innate cellular immunity. The Tim-3/Galectin-9 axis is an important regulator of Th1 cell immunity, leading to Th1 cell apoptosis. Herein, this study aims to clarify the underlying roles of the Tim-3/Galectin-9 axis in T-cell immunity in PTB. Peripheral blood mononuclear cells (PBMCs) were extracted from subjects with and without PTB to examine the expression of CD4, CD8, CD25, and Tim-3 under the stimulation of Mycobacterium tuberculosis (MTB) and purified protein derivative (PPD). In addition, the expression of Tim-3 and Galectin-9 in PBMCs was determined. The Tim-3/Galectin-9 axis in the PBMCs was activated or blocked to detect the secreted levels of IFN-γ, TNF-α, IL-2, and IL-22. MTB stimulation increased the expression of CD4, CD8, CD25, Tim-3, and Galectin-9 in PBMCs. The blockade of Tim-3/Galectin-9 axis resulted in reduced secretion of IFN-γ, TNF-α, IL-2, and IL-22 from T-cells. Moreover, Tim-3 + CD4 + T, Tim-3 + CD8 + , and Tim-3 + CD25 + T cells exhibited a greater ability to inhibit the replication of MTB in macrophages. Taken conjointly, the blockade of Tim-3/Galectin-9 axis inhibits the secretion of inflammatory cytokines in T-cells to regulate the T-cell immunity in PTB.

中文翻译：

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Tim-3/Galectin-9轴对肺结核T细胞免疫的调节作用

受肺结核 (PTB) 影响的患者表现出先天细胞免疫缺陷。Tim-3/Galectin-9 轴是 Th1 细胞免疫的重要调节因子，导致 Th1 细胞凋亡。在此，本研究旨在阐明 Tim-3/Galectin-9 轴在 PTB 中 T 细胞免疫中的潜在作用。在结核分枝杆菌 (MTB) 和纯化蛋白衍生物 (PPD) 的刺激下，从患有和未患有 PTB 的受试者中提取外周血单个核细胞 (PBMC)，以检查 CD4、CD8、CD25 和 Tim-3 的表达。此外，还测定了 PBMC 中 Tim-3 和 Galectin-9 的表达。激活或阻断 PBMC 中的 Tim-3/Galectin-9 轴以检测 IFN-γ、TNF-α、IL-2 和 IL-22 的分泌水平。MTB 刺激增加了 PBMC 中 CD4、CD8、CD25、Tim-3 和 Galectin-9 的表达。Tim-3/Galectin-9 轴的阻断导致 T 细胞分泌 IFN-γ、TNF-α、IL-2 和 IL-22 减少。此外，Tim-3 + CD4 + T、Tim-3 + CD8 + 和Tim-3 + CD25 + T 细胞表现出更强的抑制MTB 在巨噬细胞中复制的能力。同时，Tim-3/Galectin-9 轴的阻断抑制了 T 细胞中炎性细胞因子的分泌，从而调节了 PTB 中的 T 细胞免疫。