Cavanaugh Victoria J, Raulet David H, Campbell Ann E
Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA 23501, USA.
Department of Molecular and Cell Biology, and Cancer Research Laboratory, University of California, Berkeley, CA 94720, USA.
J Gen Virol. 2007 May;88(Pt 5):1440-1445. doi: 10.1099/vir.0.82444-0.
Following acute infection, murine cytomegalovirus (MCMV) replicates persistently in the salivary glands, despite the vigorous response of activated CD8 T cells that infiltrate this gland. Virus-specific CD8 T lymphocytes isolated from this organ were found to express the inhibitory CD94/NKG2A receptor that, in some virus models, confers an inhibitory response to cytotoxic T lymphocytes (CTLs). In response to MCMV infection, expression of the CD94/NKG2A ligand, Qa-1b, increased dramatically in the submandibular gland (SMG) prior to upregulation of H-2Dd. However, there was no net negative impact on virus-specific T-cell function, as virus titres were similar in CD94- and CD94+ mice. CD94/NKG2A expression, also known to inhibit apoptosis, did not influence the numbers of accumulated T, NK and NK T cells. These data indicate that expression of inhibitory CD94/NKG2A receptors does not account for the failure of MCMV-specific CTLs to clear the SMG of infection.
急性感染后，小鼠巨细胞病毒（MCMV）持续在唾液腺中复制，尽管有大量活化的CD8 T细胞浸润该腺体并产生强烈反应。从该器官分离出的病毒特异性CD8 T淋巴细胞被发现表达抑制性CD94/NKG2A受体，在某些病毒模型中，该受体赋予细胞毒性T淋巴细胞（CTL）抑制性反应。针对MCMV感染，在H-2Dd上调之前，CD94/NKG2A配体Qa-1b在颌下腺（SMG）中的表达显著增加。然而，对病毒特异性T细胞功能没有净负面影响，因为CD94基因敲除小鼠和野生型小鼠中的病毒滴度相似。已知CD94/NKG2A的表达也可抑制细胞凋亡，但它并不影响积累的T细胞、自然杀伤细胞（NK）和自然杀伤T细胞的数量。这些数据表明，抑制性CD94/NKG2A受体的表达并不能解释MCMV特异性CTL清除SMG感染失败的原因。
