Tsukaguchi K, Okamura H, Tokuyama T, Okamoto Y, Fu A, Yamamoto C, Nakaya M, Kobayashi A, Yoneda T, Narita N
Second Department of Internal Medicine Nara Medical University, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1997 Dec;35(12):1330-7.
We demonstrated that CD4+ alpha beta (CD4+) and gamma delta T cell subsets from healthy donors had similar effector functions (cytotoxicity and cytokine production) in response to mycobacterial antigens, despite differences in the antigens recognized. To elucidate the pathogenesis of pulmonary tuberculosis, this study was undertaken to compare T cell functions between patients with pulmonary tuberculosis with no complications and healthy controls. Both resting and activated CD4+ and gamma delta T cells from the patient group proliferated in response to live BCG at a significantly lower rate than those from the control group. The cytotoxicity of BCG-pulsed monocytes and IFN-gamma production in both the CD4+ and gamma delta T cells from patients was significantly lower than those of controls. In contrast to IFN-gamma, significantly higher IL-10 production by both CD4+ and gamma delta T cells from patients was detected. The proliferative responses to BCG by CD4+ and gamma delta T cells from patients after antituberculous therapy were partially restored, but remained at lower levels compared with controls. These results suggest that not only a general deterioration in CD4+ and gamma delta T cells effector functions, but also suppressive factors (such as IL-10) might be responsible for the pathogenesis of pulmonary tuberculosis, and that the low response to BCG by both CD4+ and gamma delta T cells in patients with tuberculosis is in part attributable to patient predisposition.
我们证明，尽管识别的抗原存在差异，但来自健康供体的CD4+αβ（CD4+）和γδT细胞亚群在对分枝杆菌抗原的反应中具有相似的效应功能（细胞毒性和细胞因子产生）。为了阐明肺结核的发病机制，本研究旨在比较无并发症的肺结核患者和健康对照者之间的T细胞功能。患者组静息和活化的CD4+和γδT细胞对活卡介苗的增殖反应率明显低于对照组。患者的卡介苗脉冲单核细胞的细胞毒性以及CD4+和γδT细胞中的IFN-γ产生均明显低于对照组。与IFN-γ相反，检测到患者的CD4+和γδT细胞产生的IL-10明显更高。抗结核治疗后患者的CD4+和γδT细胞对卡介苗的增殖反应部分恢复，但与对照组相比仍处于较低水平。这些结果表明，不仅CD4+和γδT细胞效应功能普遍恶化，而且抑制因子（如IL-10）可能是肺结核发病机制的原因，并且结核病患者中CD4+和γδT细胞对卡介苗的低反应部分归因于患者的易感性。
