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结核病发病机制中的免疫 - 内分泌成分。

The immuno-endocrine component in the pathogenesis of tuberculosis.

作者信息

Bottasso O, Bay M L, Besedovsky H, del Rey A

机构信息

Instituto de Inmunología, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Rosario, Argentina.

出版信息

Scand J Immunol. 2007 Aug-Sep;66(2-3):166-75. doi: 10.1111/j.1365-3083.2007.01962.x.

Abstract

Tuberculosis (TB) may be regarded as a disease in which the immune response to Mycobacterium tuberculosis, its etiologic agent, is engaged both in protection and pathology. Different T-lymphocyte subsets are involved in the immune response against M. tuberculosis, but production of interferon-gamma (IFN-gamma) by T cells seems to be fundamental for disease control. Th1-type cytokine responses predominate in patients with mild or moderate forms of pulmonary TB, whereas the production of Th2-type cytokines prevails in the severe disease. Since the immune response fails to definitely eradicate the pathogen, a chronic infection is established, and it is likely that a broad range of regulatory mechanisms operate in this situation. Cytokines released during the course of an immune response activate the hypothalamus-pituitary-adrenal axis leading to the production of glucocorticoids and dehydroepiandrosterone (DHEA), with known immunomodulatory effects. TB patients exhibit increased concentrations of interleukin-6 and cortisol in plasma, reduced DHEA and testosterone levels, together with remarkably increased growth hormone concentrations that were not accompanied by an expected raise in insulin-like growth factor-1. Significant increases in estradiol, prolactin, and thyroid hormone concentrations were also detected in patients. Cortisol inhibits the mycobacterial antigen-driven proliferation and IFN-gamma production, whereas DHEA suppresses transforming growth factor beta production by lymphoid cells from TB patients with advanced disease. Furthermore, supernatants from cultures of M. tuberculosis-stimulated mononuclear cells of TB patients inhibit DHEA secretion by a human adrenal cell line. This type of immuno-endocrine interactions may affect the control of tissue damage and the development of protective immune responses, partly accounting for disease aggravation.

摘要

结核病(TB)可被视为一种疾病,在该疾病中,机体对其病原体结核分枝杆菌的免疫反应既参与了保护作用,也导致了病理变化。不同的T淋巴细胞亚群参与了针对结核分枝杆菌的免疫反应,但T细胞产生干扰素-γ(IFN-γ)似乎对疾病控制至关重要。在轻度或中度肺结核患者中,Th1型细胞因子反应占主导,而在严重疾病中,Th2型细胞因子的产生更为普遍。由于免疫反应未能彻底根除病原体,从而形成了慢性感染,在这种情况下可能有多种调节机制发挥作用。免疫反应过程中释放的细胞因子激活下丘脑-垂体-肾上腺轴,导致糖皮质激素和脱氢表雄酮(DHEA)的产生,它们具有已知的免疫调节作用。结核病患者血浆中白细胞介素-6和皮质醇浓度升高,DHEA和睾酮水平降低,同时生长激素浓度显著升高,而胰岛素样生长因子-1却未如预期升高。患者体内雌二醇、催乳素和甲状腺激素浓度也有显著升高。皮质醇抑制分枝杆菌抗原驱动的增殖和IFN-γ的产生,而DHEA抑制晚期结核病患者淋巴细胞产生转化生长因子β。此外,结核分枝杆菌刺激的结核病患者单核细胞培养上清液抑制人肾上腺细胞系分泌DHEA。这种免疫-内分泌相互作用可能会影响组织损伤的控制和保护性免疫反应的发展,部分解释了疾病的加重。

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