Kuwata Takeo, Nishimura Yoshiaki, Whitted Sonya, Ourmanov Ilnour, Brown Charles R, Dang Que, Buckler-White Alicia, Iyengar Ranjini, Brenchley Jason M, Hirsch Vanessa M
Priority Organization for Innovation and Excellence, Kumamoto University, Kumamoto, Japan.
PLoS Pathog. 2009 Apr;5(4):e1000372. doi: 10.1371/journal.ppat.1000372. Epub 2009 Apr 10.
The progressive decline of CD4(+) T cells is a hallmark of disease progression in human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infection. Whereas the acute phase of the infection is dominated by virus-mediated depletion of memory CD4(+) T cells, chronic infection is often associated with a progressive decline of total CD4(+) T cells, including the naïve subset. The mechanism of this second phase of CD4(+) T cell loss is unclear and may include immune activation-induced cell death, immune-mediated destruction, and regenerative or homeostatic failure. We studied patterns of CD4(+) T cell subset depletion in blood and tissues in a group of 20 rhesus macaques inoculated with derivatives of the pathogenic SIVsmE543-3 or SIVmac239. Phenotypic analysis of CD4(+) T cells demonstrated two patterns of CD4(+) T cell depletion, primarily affecting either naïve or memory CD4(+) T cells. Progressive decline of total CD4(+) T cells was observed only in macaques with naïve CD4(+) T cell depletion (ND), though the depletion of memory CD4(+) T cells was profound in macaques with memory CD4(+) T cell depletion (MD). ND macaques exhibited lower viral load and higher SIV-specific antibody responses and greater B cell activation than MD macaques. Depletion of naïve CD4(+) T cells was associated with plasma antibodies autoreactive with CD4(+) T cells, increasing numbers of IgG-coated CD4(+) T cells, and increased incidence of autoreactive antibodies to platelets (GPIIIa), dsDNA, and phospholipid (aPL). Consistent with a biological role of these antibodies, these latter antibodies were accompanied by clinical features associated with autoimmune disorders, thrombocytopenia, and catastrophic thrombotic events. More importantly for AIDS pathogenesis, the level of autoreactive antibodies significantly correlated with the extent of naïve CD4(+) T cell depletion. These results suggest an important role of autoreactive antibodies in the CD4(+) T cell decline observed during progression to AIDS.
CD4(+) T细胞的逐渐减少是人类免疫缺陷病毒(HIV)和猴免疫缺陷病毒(SIV)感染中疾病进展的一个标志。在感染的急性期,病毒介导的记忆性CD4(+) T细胞耗竭占主导,而慢性感染通常与包括初始亚群在内的总CD4(+) T细胞的逐渐减少有关。CD4(+) T细胞损失第二阶段的机制尚不清楚,可能包括免疫激活诱导的细胞死亡、免疫介导的破坏以及再生或稳态功能障碍。我们研究了一组接种致病性SIVsmE543 - 3或SIVmac239衍生物的20只恒河猴血液和组织中CD4(+) T细胞亚群的耗竭模式。CD4(+) T细胞的表型分析显示出两种CD4(+) T细胞耗竭模式,主要影响初始或记忆性CD4(+) T细胞。仅在初始CD4(+) T细胞耗竭(ND)的猕猴中观察到总CD4(+) T细胞的逐渐减少,尽管在记忆性CD4(+) T细胞耗竭(MD)的猕猴中记忆性CD4(+) T细胞的耗竭也很严重。与MD猕猴相比,ND猕猴表现出更低的病毒载量、更高的SIV特异性抗体反应以及更强的B细胞激活。初始CD4(+) T细胞的耗竭与针对CD4(+) T细胞的自身反应性血浆抗体、IgG包被的CD4(+) T细胞数量增加以及针对血小板(GPIIIa)、双链DNA和磷脂(aPL)的自身反应性抗体发生率增加有关。与这些抗体的生物学作用一致,后一种抗体伴有与自身免疫性疾病、血小板减少症和灾难性血栓形成事件相关的临床特征。对于艾滋病发病机制更重要的是,自身反应性抗体的水平与初始CD4(+) T细胞耗竭的程度显著相关。这些结果表明自身反应性抗体在艾滋病进展过程中观察到的CD4(+) T细胞减少中起重要作用。