INTERFERON-INDEPENDENT INCREASES IN CLASS-I MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGEN EXPRESSION FOLLOW FLAVIVIRUS INFECTION
INTERFERON-INDEPENDENT INCREASES IN CLASS-I MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGEN EXPRESSION FOLLOW FLAVIVIRUS INFECTION
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DOI：
10.1099/0022-1317-69-10-2535
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发表时间：
1988-10-01
影响因子：
3.8
通讯作者：
KESSON, AM
中科院分区：
文献类型：
--
作者：
KING, NJC;KESSON, AM
四个黄病毒，西尼罗河病毒（WNV），昆津，墨累谷脑炎和日本B脑炎，导致在6至10倍的增加，个别H-2K和H-2D I类主要组织相容性复合体（MHC）抗原的表达后，感染第三代小鼠胚胎成纤维细胞16至48小时。黄病毒增加抗原表达的机制尚未完全阐明，但似乎部分独立于干扰素-β介导。 （IFN-β）分泌，如抗IFN-α。β的抗体部分抑制了WNV诱导的增加，但完全阻止了由加入（i）纯IFN-β，(ii)IFN-β-含有来自WNV感染的小鼠胚胎成纤维细胞（MEF）的上清液，或（iii）聚肌苷酸-聚胞苷酸。放线菌素D处理MEF，抑制mRNA合成> 90%，通过[3 H]尿苷摄取测定，完全抑制了由WNV感染引起的MHC表达增加。因此，感染后I类MHC抗原表达的增加依赖于细胞RNA合成。
Infection of tertiary-passaged mouse embryo fibroblasts by four flaviviruses, West Nile (WNV), Kunjin, Murray Valley encephalitis and Japanese B encephalitis, resulted in a six- to 10-fold increase in the expression of individual H-2K and H-2D class I major histocompatibility complex (MHC) antigens 16 to 48 h after infection. The mechanism(s) by which flaviviruses increased antigen expression has not been fully elucidated, but appears to be mediated partly independently of interferon-.beta. (IFN-.beta.) secretion, as anti-IFN-.alpha..beta. antibodies partially inhibited the WNV-induced increase but totally prevented increases caused by the addition of (i) pure IFN-.beta., (ii) IFN-.beta.-containing supernatants from WNV-infected mouse embryo fibroblasts (MEF), or (iii) polyinosinic-polycytidylic acid. Actinomycin D treatment of MEF, which inhibited mRNA synthesis by > 90% as determined by [3H]uridine uptake, totally inhibited the increased MHC expression caused by WNV infection. Thus, the increase in class I MHC antigen expression following infection is dependent upon cellular RNA synthesis.