Major histocompatibility complex class I-restricted cytotoxic T 1 lymphocyte responses during primary simian immunodeficiency virus infection in Burmese rhesus macaques.

Major histocompatibility complex class I-restricted cytotoxic T 1 lymphocyte responses during primary simian immunodeficiency virus infection in Burmese rhesus macaques.
复制标题

缅甸恒河猴原发性猿猴免疫缺陷病毒感染期间主要组织相容性复合物 I 类限制细胞毒性 T 1 淋巴细胞反应。

DOI:
10.1111/j.1348-0421.2011.00384.x
复制
发表时间:
2011
期刊:
Microbiol. Immunol.
影响因子:
--
通讯作者:
M.
M.
中科院分区:
--
文献类型:
--
作者:
Nakamura;M.

文献摘要

相似文献

主要组织相容性复合物I类(MHC-I)限制性CD 8+细胞毒性T淋巴细胞(CTL)反应对于控制人类免疫缺陷病毒(HIV)和猿猴免疫缺陷病毒(SIV)复制至关重要。特别是,Gag特异性CTL应答已显示对HIV/SIV复制施加强抑制压力。此外,最近有人提出Vif特异性CTL频率与体外抗SIV疗效相关。宿主MHC-I基因型可能影响这些有效CTL应答的免疫优势模式。在这里,在三组缅甸恒河猴中检查了原发性SIVmac 239感染期间Gag和Vif特异性CTL应答,每组具有不同的MHC-I单倍型。第一组四只猕猴,具有MHC-I单倍型90 - 010-Ie,没有显示Gag-或Vif-特异性CTL应答。然而,Nef特异性CTL应答被激发,表明原发性SIV感染并不诱导对由90 - 010-Ie-衍生的MHC-I分子限制的Gag/Vif表位特异的主要CTL应答。相反,在第二组两只89 - 075-Iw-阳性动物和第三组两只91 - 010-Is-阳性动物中诱导了Gag-和Vif-特异性CTL应答。考虑到预防性疫苗接种可能影响病毒暴露后CTL免疫优势,这些猕猴组可用于评价疫苗抗原特异性CTL对SIV感染的有效性。
Major histocompatibility complex class I (MHC‐I)‐restricted CD8+cytotoxic T lymphocyte (CTL) responses are crucial for the control of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) replication. In particular, Gag‐specific CTL responses have been shown to exert strong suppressive pressure on HIV/SIV replication. Additionally, association of Vif‐specific CTL frequencies within vitroanti‐SIV efficacy has been suggested recently. Host MHC‐I genotypes could affect the immunodominance patterns of these potent CTL responses. Here, Gag‐ and Vif‐specific CTL responses during primary SIVmac239 infection were examined in three groups of Burmese rhesus macaques, each group having a different MHC‐I haplotype. The first group of four macaques, which possessed the MHC‐I haplotype90‐010‐Ie, did not show Gag‐ or Vif‐specific CTL responses. However, Nef‐specific CTL responses were elicited, suggesting that primary SIV infection does not induce predominant CTL responses specific for Gag/Vif epitopes restricted by90‐010‐Ie‐derived MHC‐I molecules. In contrast, Gag‐ and Vif‐specific CTL responses were induced in the second group of two89‐075‐Iw‐positive animals and the third group of two91‐010‐Is‐positive animals. Considering the potential of prophylactic vaccination to affect CTL immunodominance post‐viral exposure, these groups of macaques would be useful for evaluation of vaccine antigen‐specific CTL efficacy against SIV infection.