Mariani F, Goletti D, Ciaramella A, Martino A, Colizzi V, Fraziano M
Experimental Medicine Institute--Rome, Italy.
Curr Mol Med. 2001 May;1(2):209-16. doi: 10.2174/1566524013363933.
Human macrophages represent the first line of defense for the containment of Mycobacterium tuberculosis infection. After phagocytosis, macrophages express activation surface markers and produce proinflammatory cytokines and chemokines whose main role is to control pathogen spreading by recruiting peripheral lymphocytes and monocytes at the site of inflammation. However, in the case of a concomitant human immunodeficiency virus (HIV) infection, these signals strongly enhance the susceptibility to viral infection both at the viral entry and replication levels. Under these conditions, viral expansion extends beyond tissue macrophages to T cells and vice-versa, according to the emerging viral phenotype. In absence of an efficient immune response, Mycobacterium tuberculosis can replicate in macrophages in an uncontrolled fashion culminating in macrophage death by apoptosis. As a consequence, a more severe form of immunedepression, involving both innate and specific immune responses, could be responsible for both ematogenous mycobacterial dissemination and extrapulmonary form of tuberculosis in HIV-infected patients.
人类巨噬细胞是遏制结核分枝杆菌感染的第一道防线。吞噬作用后，巨噬细胞表达激活表面标志物并产生促炎细胞因子和趋化因子，其主要作用是通过在炎症部位募集外周淋巴细胞和单核细胞来控制病原体传播。然而，在同时感染人类免疫缺陷病毒（HIV）的情况下，这些信号在病毒进入和复制水平上都强烈增强了对病毒感染的易感性。在这些条件下，根据新出现的病毒表型，病毒扩展不仅超出组织巨噬细胞，还扩展到T细胞，反之亦然。在缺乏有效免疫反应的情况下，结核分枝杆菌可在巨噬细胞中不受控制地复制，最终导致巨噬细胞凋亡死亡。因此，涉及先天免疫和特异性免疫反应的更严重形式的免疫抑制，可能是导致HIV感染患者血行播散性分枝杆菌病和肺外结核的原因。
