Suppr超能文献

来自感染猿猴/人类免疫缺陷病毒的恒河猴的HIV-1包膜特异性CD4 +辅助性T细胞识别受MHC II类DRB1*0406和DRB*W201分子限制的表位。

HIV-1 envelope-specific CD4+ T helper cells from simian/human immunodeficiency virus-infected rhesus monkeys recognize epitopes restricted by MHC class II DRB1*0406 and DRB*W201 molecules.

作者信息

Lekutis C, Letvin N L

机构信息

Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.

出版信息

J Immunol. 1997 Aug 15;159(4):2049-57.

PMID:9257873
Abstract

The HIV-1 envelope (Env)-specific Th cell response of rhesus monkeys infected with nonpathogenic chimeric simian/human immunodeficiency viruses (SHIV) was assessed at a molecular level by establishing rgp120-specific CD4+ T cell lines. Epitopes recognized by these MHC class II-restricted Th cells were identified within the second (C2), third (C3), and fifth (C5) conserved regions of HIV-1 gp120. The epitope located in C2 was found to be restricted by the rhesus monkey (Macaca mulatta) leukocyte Ag Mamu-DRB10406, and the Th cell epitope in C5 was found to be restricted by Mamu-DRBW201. The restriction element requirements of the C2 and C5 epitope-specific CD4+ Th cells appear to be rather stringent, because these peptide epitopes were not recognized in the presence of other Mamu-DR expressing cell lines. The ability to analyze HIV-1 Env-specific CD4+ T cell responses in SHIV-infected monkeys will enhance the utility of this model for studying AIDS pathogenesis and for assessing novel HIV-1 vaccine strategies.

摘要

通过建立重组 gp120 特异性 CD4+ T 细胞系,在分子水平评估感染非致病性嵌合猿猴/人类免疫缺陷病毒(SHIV)的恒河猴的 HIV-1 包膜(Env)特异性 Th 细胞反应。在 HIV-1 gp120 的第二个(C2)、第三个(C3)和第五个(C5)保守区域内鉴定出这些 MHC II 类限制性 Th 细胞识别的表位。发现位于 C2 的表位受恒河猴(猕猴)白细胞抗原 Mamu-DRB10406 限制,C5 中的 Th 细胞表位受 Mamu-DRBW201 限制。C2 和 C5 表位特异性 CD4+ Th 细胞的限制元件要求似乎相当严格,因为在存在其他表达 Mamu-DR 的细胞系时,这些肽表位未被识别。分析 SHIV 感染猴子中 HIV-1 Env 特异性 CD4+ T 细胞反应的能力将提高该模型在研究艾滋病发病机制和评估新型 HIV-1 疫苗策略方面的实用性。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验