Suppr超能文献

一种针对人类免疫缺陷病毒1型p24保守表位的CD4+细胞毒性T淋巴细胞克隆:细胞毒性活性以及白细胞介素-2和白细胞介素-6的分泌

A CD4+ cytotoxic T-lymphocyte clone to a conserved epitope on human immunodeficiency virus type 1 p24: cytotoxic activity and secretion of interleukin-2 and interleukin-6.

作者信息

Littaua R A, Oldstone M B, Takeda A, Ennis F A

机构信息

Department of Medicine, University of Massachusetts Medical Center, Worcester 01655.

出版信息

J Virol. 1992 Jan;66(1):608-11. doi: 10.1128/JVI.66.1.608-611.1992.

Abstract

A CD4+ cytotoxic T-lymphocyte (CTL) clone, established from the peripheral blood of a human immunodeficiency virus (HIV)-seropositive donor, lysed autologous target cells that were infected with a recombinant vaccinia virus containing the gag gene of HIV type 1 and target cells pulsed with p24gag construct expressed in Escherichia coli. The recognition of the HLA-DQ-restricted epitope by this clone was further defined by using overlapping synthetic peptides. The epitope recognized by this CD4+ CTL clone (amino acids 140 to 148) overlaps with a CD8+ epitope and is highly conserved among all isolates of HIV type 1 that have been sequenced. Production and secretion of lymphokines such as interleukin-2 and interleukin-6 after specific antigenic stimulation were demonstrated by this gag-specific CD4+ CTL clone.

摘要

从一名人类免疫缺陷病毒(HIV)血清反应阳性供体的外周血中建立的一个CD4 + 细胞毒性T淋巴细胞(CTL)克隆,裂解了被含有1型HIV gag基因的重组痘苗病毒感染的自体靶细胞,以及用在大肠杆菌中表达的p24gag构建体脉冲处理过的靶细胞。通过使用重叠合成肽进一步确定了该克隆对HLA - DQ限制表位的识别。这个CD4 + CTL克隆识别的表位(氨基酸140至148)与一个CD8 + 表位重叠,并且在所有已测序的1型HIV分离株中高度保守。这个gag特异性CD4 + CTL克隆证明了在特异性抗原刺激后白细胞介素 - 2和白细胞介素 - 6等淋巴因子的产生和分泌。

相似文献

8
Effective lysis of HIV-1-infected primary CD4+ T cells by a cytotoxic T-lymphocyte clone directed against a novel A2-restricted reverse-transcriptase epitope.
J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Oct 1;19(2):111-20. doi: 10.1097/00042560-199810010-00002.

引用本文的文献

本文引用的文献

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