RESUMEN
Objective:To investigate the changes of T-lymphocyte subsets, T-cell immunoglobulin and mucin domain molecule-1 (TIM-1) and TIM-3 levels, and cytokines in the peripheral blood of patients with active tuberculosis.Methods:From December 2017 to December 2018, 50 tuberculosis patients and 50 cured tuberculosis patients in Zhejiang Hospital of Integrated Chinese and Western Medicine were selected as the tuberculosis group and cured tuberculosis group, respectively. Fifty healthy individuals in the same period were selected as the control group. Flow cytometry was used to detect the T-lymphocyte subsets in the peripheral blood. The mRNA levels of TIM-1, TIM-3, interferon(IFN)-γ and interleukin(IL)-4 in peripheral blood mononuclear cells (PBMC) were detected by quantitative real-time polymerase chain reacticn (PCR). T test was used for statistical analysis. Results:The ratio of CD4 + /CD8 + T lymphocytes in the tuberculosis group (1.21±0.50) decreased significantly, comparing with those in the cured tuberculosis group (1.88±0.62) and the control group (1.92±0.82). The differences were statistically significant ( t=2.148 and 2.207, respectively, both P<0.05). The mRNA levels of TIM-1, TIM-3 and IL-4 in PBMC in the tuberculosis group were 2.16±0.37, 1.59±0.36 and 1.52±0.69, respectively, which were all higher than those in the cured tuberculosis group (1.60±1.23, 1.01±0.52 and 0.91±0.36, respectively) and the healthy control group (1.40±0.27, 0.92±0.34 and 0.79±0.42, respectively). All of these differences were statistically significant ( t=14.120, 11.440, 17.130, 12.090, 12.050 and 17.030, respectively, all P<0.05). However, the IFN-γ mRNA level (0.43±0.11) was lower than that in the cured tuberculosis group (1.74±0.72) and the control group (1.82±1.17), and the differences were both statistically significant ( t=13.880 and 11.430, respectively, both P<0.05). Conclusion:The immune dysfunction in patients with active tuberculosis may be related to the low ratio of CD4 + /CD8 + T lymphocytes, the increased expressions of TIM-1 and TIM-3, and the imbalance of helper T lymphocyte (Th)1/Th2 cytokines.