Slater J S, Futch W S, Cavanaugh V J, Campbell A E
Department of Microbiology and Immunology, Eastern Virginia Medical School, Norfolk 23501.
Virology. 1991 Nov;185(1):132-9. doi: 10.1016/0042-6822(91)90761-y.
Murine cytomegalovirus (MCMV) inhibits antigen-specific cytotoxic T lymphocyte (CTL) priming in vivo (Campbell et al., 1989). To address the mechanism of this immune suppression, two possibilities were considered: (1) MCMV directly interferes with in vivo priming of CTL precursors (CTLp), or (2) MCMV suppresses T helper cell functions necessary for CTL priming. We therefore quantitated T helper cell function in MCMV-infected, SV40-immune mice and assessed dependency of SV40-specific CTLp priming on T helper cell activity. MCMV infection of H-2b mice significantly suppressed the frequency of IL-2 producing T helper cells generated in SV40-immune mice. This suppression was not due to alterations in the number or percentage of CD4 lymphocytes. The helper cell deficiency correlated with suppressed SV40-specific CTL activity. However, CTLp priming in vivo was found to be independent of CD4 T helper cells and IL-2. Therefore, the suppressive effects of MCMV on helper and cytotoxic T cell functions are independent, implying that MCMV directly inhibits an event in lymphocyte priming common to both helper and cytotoxic T cells.
小鼠巨细胞病毒（MCMV）在体内抑制抗原特异性细胞毒性T淋巴细胞（CTL）的致敏（坎贝尔等人，1989年）。为了探究这种免疫抑制的机制，考虑了两种可能性：（1）MCMV直接干扰CTL前体细胞（CTLp）在体内的致敏，或（2）MCMV抑制CTL致敏所需的T辅助细胞功能。因此，我们对感染MCMV的SV40免疫小鼠的T辅助细胞功能进行了定量，并评估了SV40特异性CTLp致敏对T辅助细胞活性的依赖性。H-2b小鼠感染MCMV显著抑制了SV40免疫小鼠中产生白细胞介素-2的T辅助细胞的频率。这种抑制并非由于CD4淋巴细胞数量或百分比的改变。辅助细胞缺陷与SV40特异性CTL活性的抑制相关。然而，发现体内CTLp致敏不依赖于CD4 T辅助细胞和白细胞介素-2。因此，MCMV对辅助性和细胞毒性T细胞功能的抑制作用是独立的，这意味着MCMV直接抑制了辅助性和细胞毒性T细胞共有的淋巴细胞致敏过程中的一个事件。
