MHC class I up-regulation by flaviviruses:: Immune interaction with unknown advantage to host or pathogen
MHC class I up-regulation by flaviviruses:: Immune interaction with unknown advantage to host or pathogen
复制标题
DOI：
10.1046/j.1440-1711.2003.01161.x
复制
发表时间：
2003-06-01
影响因子：
4
通讯作者：
Regner, M
中科院分区：
文献类型：
--
作者：
Lobigs, M;M端llbacher, A;Regner, M
与许多其他病毒通过下调主要组织相容性复合体I类限制性抗原提呈来逃避细胞毒性T细胞识别不同，黄病毒感染哺乳动物细胞可上调主要组织相容性复合体I类分子在细胞表面的表达。本文综述了黄病毒诱导的主要组织相容性复合体I类基因上调的两种可能机制，一种是通过激活转录因子NF-kappaB，另一种是通过增加内质网腔内肽的输入，并讨论了黄病毒介导的现象对自然杀伤细胞和细胞毒性T细胞识别靶细胞的生物学效应。最后，在黄病毒在脊椎动物宿主和节肢动物载体之间传播的生物学背景下，我们推测了黄病毒介导的主要组织相容性复合体I类抗原提呈的生理作用，并暗示它可能代表了一种免疫逃避自然杀伤细胞反应的策略，或者，作为替代，主要组织相容性复合体I类的上调是黄病毒复制的副产品，对病毒生长没有意义。
In contrast to many other viruses that escape from cytotoxic T cell recognition by down-regulating major histocompatibility complex class I-restricted antigen presentation, flavivirus infection of mammalian cells up-regulates cell surface expression of major histocompatibility complex class I molecules. Two putative mechanisms for flavivirus-induced major histocompatibility complex class I up-regulation, one via activation of the transcription factor NF-kappaB, the second by augmentation of peptide import into the lumen of the endoplasmic reticulum, are reviewed, and the biological effect of the flavivirus-mediated phenomenon on target cell recognition by natural killer and cytotoxic T cells is addressed. Finally, we speculate on the physiological role of flavivirus-mediated modulation of major histocompatibility complex class I antigen presentation in the context of the biology of flavivirus transmission between the vertebrate host and arthropod vector and suggest that it may represent a strategy for immune evasion from the natural killer cell response or, alternatively, that up-regulation of major histocompatibility complex class I is a by-product of flavivirus replication without significance for virus growth.