Tesselaar Kiki, Arens Ramon, van Schijndel Gijs M W, Baars Paul A, van der Valk Martin A, Borst Jannie, van Oers Marinus H J, van Lier René A W
Laboratory for Experimental Immunology, Academic Medical Center, P.O. Box 22700, 1100DD Amsterdam, The Netherlands.
Nat Immunol. 2003 Jan;4(1):49-54. doi: 10.1038/ni869. Epub 2002 Dec 9.
It has been proposed that HIV-1, in addition to directly infecting and killing CD4+ T cells, causes T cell dysfunction and T cell loss by chronic immune activation. We analyzed the effects of chronic immune activation in mice that constitutively expressed CD70, the ligand for the tumor necrosis factor receptor family member CD27, on B cells. CD70 transgenic (CD70 Tg) mice showed a progressive conversion of naive T cells into effector-memory cells, which culminated in the depletion of naive T cells from lymph nodes and spleen. T cell changes depended on continuous CD27-CD70 interactions and T cell antigen receptor stimulation. Despite this hyperactive immune system, CD70 Tg mice died aged 6-8 months from Pneumocystis carinii infection, a hallmark of T cell immunodeficiency. Thus, persistent delivery of costimulatory signals via CD27-CD70 interactions, as may occur during chronic active viral infections, can exhaust the T cell pool and is sufficient to induce lethal immunodeficiency.
有人提出,除了直接感染和杀死CD4+ T细胞外,HIV-1还通过慢性免疫激活导致T细胞功能障碍和T细胞损失。我们分析了在组成性表达肿瘤坏死因子受体家族成员CD27的配体CD70的小鼠中,慢性免疫激活对B细胞的影响。CD70转基因(CD70 Tg)小鼠表现出幼稚T细胞逐渐转化为效应记忆细胞,最终导致淋巴结和脾脏中的幼稚T细胞耗竭。T细胞变化取决于持续的CD27-CD70相互作用和T细胞抗原受体刺激。尽管免疫系统过度活跃,但CD70 Tg小鼠在6-8个月大时死于卡氏肺孢子虫感染,这是T细胞免疫缺陷的一个标志。因此,如在慢性活动性病毒感染期间可能发生的那样,通过CD27-CD70相互作用持续传递共刺激信号,可耗尽T细胞库,并足以诱导致命的免疫缺陷。