Seitzer U, Kayser K, Höhn H, Entzian P, Wacker H H, Ploetz S, Flad H D, Gerdes J, Maeurer M J
Division of Immunology and Cell Biology, Research Center Borstel, Borstel, Germany.
Immunology. 2001 Nov;104(3):269-77. doi: 10.1046/j.1365-2567.2001.01323.x.
Control of mycobacterial infection by the cellular immune system relies both on antigen-presenting cells and on T lymphocytes. The quality of an effective cellular immune response is dependent on functional signal transduction residing in the cytoplasmic tails of the T-cell receptor CD3 components. In order to investigate potential effects of mycobacteria on T-cell receptor signalling, we examined the protein expression of T-cell signal transduction molecules (CD3zeta, ZAP-70, p59fyn, p56lck). In Western blots of peripheral blood mononuclear cells of Mycobacterium tuberculosis infected patients, only the CD3zeta-chain showed a marked reduction in protein expression. To investigate the situation in situ, immunoenzymatic and immunofluorescence stainings for CD3epsilon and CD3zeta expression were performed on sections of normal lymphoid tissue, M. leprae infected and sarcoid tissue. CD3epsilon and CD3zeta expression were similar with respect to intensity, localization and the number of cells stained in normal lymphoid tissue and in sarcoid granulomas. In contrast, the granulomas of M. leprae infected tissues showed a significantly reduced expression of CD3zeta compared to CD3epsilon. Using double immunofluorescence analysis, virtually no CD3zeta expression could be detected in comparison to the CD3epsilon expression in the lesions. Apparently, mycobacteria are capable of significantly reducing CD3zeta-chain expression, which may be restored by cytokines. IL-2-enhanced zeta-chain expression and T-cell effector functions, defined by interferon-gamma release, in M. tuberculosis-specific and human leucocyte antigen-DR restricted CD4+ T cells isolated from granuloma lesions from patients with pulmonary tuberculosis. Because CD3zeta is essential for CD3 signalling and for eliciting T-cell effector functions, reduced CD3zeta protein expression could result in altered signal transduction and inefficient T-cell effector functions. Alternatively, reduced CD3zeta-chain expression may protect T cells from repetitive TCR stimulation associated with anergy or apoptosis.
细胞免疫系统对分枝杆菌感染的控制依赖于抗原呈递细胞和T淋巴细胞。有效的细胞免疫反应的质量取决于T细胞受体CD3组分胞质尾部的功能性信号转导。为了研究分枝杆菌对T细胞受体信号传导的潜在影响,我们检测了T细胞信号转导分子(CD3ζ、ZAP-70、p59fyn、p56lck)的蛋白表达。在肺结核感染患者外周血单个核细胞的蛋白质印迹中,只有CD3ζ链的蛋白表达显著降低。为了研究原位情况,对正常淋巴组织、麻风杆菌感染组织和结节病组织切片进行了CD3ε和CD3ζ表达的免疫酶标和免疫荧光染色。在正常淋巴组织和结节病肉芽肿中,CD3ε和CD3ζ的表达在强度、定位和染色细胞数量方面相似。相比之下,与CD3ε相比,麻风杆菌感染组织的肉芽肿中CD3ζ的表达显著降低。使用双重免疫荧光分析,与病变中的CD3ε表达相比,几乎检测不到CD3ζ的表达。显然,分枝杆菌能够显著降低CD3ζ链的表达,而细胞因子可能会使其恢复。在从肺结核患者肉芽肿病变中分离出的结核分枝杆菌特异性和人类白细胞抗原-DR限制性CD4+T细胞中,IL-2增强了ζ链表达和由干扰素-γ释放定义的T细胞效应功能。由于CD3ζ对于CD3信号传导和引发T细胞效应功能至关重要,CD3ζ蛋白表达降低可能导致信号转导改变和T细胞效应功能低效。或者,CD3ζ链表达降低可能保护T细胞免受与无反应性或细胞凋亡相关的重复性TCR刺激。