Rheumatology Division, Department of Medicine, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA.
Proc Natl Acad Sci U S A. 2012 Nov 20;109(47):E3260-7. doi: 10.1073/pnas.1217111109. Epub 2012 Oct 29.
Although viral MHC class I inhibition is considered a classic immune-evasion strategy, its in vivo role is largely unclear. Mutant cowpox virus lacking its MHC class I inhibitors is markedly attenuated during acute infection because of CD8(+) T-cell-dependent control, but it was not known how CD8(+) T-cell responses are affected. Interestingly, we found no major effect of MHC class I down-regulation on priming of functional cowpox virus-specific CD8(+) T cells. Instead, we demonstrate that, during acute infection in vivo, MHC class I down-regulation prevents primed virus-specific CD8(+) T cells from recognizing infected cells and exerting effector responses to control the infection.
尽管病毒 MHC I 类抑制被认为是一种经典的免疫逃逸策略，但它在体内的作用在很大程度上尚不清楚。在急性感染期间，缺乏 MHC I 类抑制剂的突变牛痘病毒由于 CD8+T 细胞依赖性控制而明显减弱，但尚不清楚 CD8+T 细胞反应如何受到影响。有趣的是，我们没有发现 MHC I 下调对功能性牛痘病毒特异性 CD8+T 细胞的引发有重大影响。相反，我们证明在体内急性感染期间，MHC I 下调可防止已引发的病毒特异性 CD8+T 细胞识别感染细胞并发挥效应反应来控制感染。
