Lin Philana Ling, Rutledge Tara, Green Angela M, Bigbee Matthew, Fuhrman Carl, Klein Edwin, Flynn JoAnne L
Department of Pediatrics, Children's Hospital of Pittsburgh of the University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
AIDS Res Hum Retroviruses. 2012 Dec;28(12):1693-702. doi: 10.1089/AID.2012.0028. Epub 2012 May 4.
CD4 T cells are believed to be important in protection against Mycobacterium tuberculosis, but the relative contribution to control of initial or latent infection is not known. Antibody-mediated depletion of CD4 T cells in M. tuberculosis-infected cynomolgus macaques was used to study the role of CD4 T cells during acute and latent infection. Anti-CD4 antibody severely reduced levels of CD4 T cells in blood, airways, and lymph nodes. Increased pathology and bacterial burden were observed in CD4-depleted monkeys during the first 8 weeks of infection compared to controls. CD4-depleted monkeys had greater interferon (IFN)-γ expression and altered expression of CD8 T cell activation markers. During latent infection, CD4 depletion resulted in clinical reactivation in only three of six monkeys. Reactivation was associated with lower CD4 T cells in the hilar lymph nodes. During both acute and latent infection, CD4 depletion was associated with reduced percentages of CXCR3(+) expressing CD8 T cells, reported to be involved in T cell recruitment, regulatory function, and effector and memory T cell maturation. CXCR3(+) CD8 T cells from hilar lymph nodes had more mycobacteria-specific cytokine expression and greater coexpression of multiple cytokines compared to CXCR3(-) CD8 T cells. CD4 T cells are required for protection against acute infection but reactivation from latent infection is dependent on the severity of depletion in the draining lymph nodes. CD4 depletion influences CD8 T cell function. This study has important implications for human HIV-M. tuberculosis coinfection.
CD4 T细胞被认为在抵抗结核分枝杆菌感染中起重要作用,但对初始感染或潜伏感染控制的相对贡献尚不清楚。在感染结核分枝杆菌的食蟹猴中,通过抗体介导的方式清除CD4 T细胞,以研究CD4 T细胞在急性感染和潜伏感染期间的作用。抗CD4抗体严重降低了血液、气道和淋巴结中CD4 T细胞的水平。与对照组相比,在感染的前8周,CD4细胞耗竭的猴子出现了更严重的病理变化和更高的细菌负荷。CD4细胞耗竭的猴子有更高的干扰素(IFN)-γ表达,并且CD8 T细胞活化标志物的表达发生了改变。在潜伏感染期间,CD4细胞耗竭仅导致六只猴子中的三只出现临床再激活。再激活与肺门淋巴结中较低的CD4 T细胞有关。在急性感染和潜伏感染期间,CD4细胞耗竭都与表达CXCR3的CD8 T细胞百分比降低有关,据报道CXCR3与T细胞募集、调节功能以及效应和记忆T细胞成熟有关。与CXCR3(-)CD8 T细胞相比,来自肺门淋巴结的CXCR3(+)CD8 T细胞有更多的分枝杆菌特异性细胞因子表达和更高的多种细胞因子共表达。抵抗急性感染需要CD4 T细胞,但潜伏感染的再激活取决于引流淋巴结中细胞耗竭的严重程度。CD4细胞耗竭会影响CD8 T细胞功能。这项研究对人类HIV-结核分枝杆菌合并感染具有重要意义。