• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

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

Reactivity of HTLV-transformed human T-cell lines to MHC class II antigens.

作者信息

Suciu-Foca N, Rubinstein P, Popovic M, Gallo R C, King D W

出版信息

Nature. 1984;312(5991):275-7. doi: 10.1038/312275a0.

DOI:10.1038/312275a0
PMID:6095090
Abstract

T-cell lines established from individuals infected with human T-cell leukaemia virus (HTLV) or generated by co-cultivation of normal human T cells with HTLV-infected T-cells, express class II (HLA-D/DR or Ia) antigens of the major histocompatibility complex (MHC) and interleukin-2 (IL-2) receptors. Because the expression of these markers characterizes the differentiation of immunologically activated T cells, we have now explored the possibility that HTLV- infected T cells might be primed to autologous or allogeneic Ia antigens expressed by the infecting cells. Our studies on the capacity of HTLV-infected T cells to display responses on mixed lymphocyte culture indicate that such T cells as well as single-cell clones derived from them, react non-discriminatively to all known allelic variants of human HLA-D/DR antigens, including those expressed by the responding cells. This reaction is inhibited by antibody to human Ia and is not triggered by Ia-negative T-leukaemia cells. The structure recognized seems to be a common epitope determinant of human Ia antigens, as (HTLV-infected) T cells primed in vitro to one HLA-D/DR specificity display amplified responses to all other HLA-D/DR antigens. We therefore believe that autostimulation by a self-Ia determinant may trigger the clonal expansion of HTLV-infected T cells and potentiate autoimmune processes.

摘要

相似文献

1
Reactivity of HTLV-transformed human T-cell lines to MHC class II antigens.
Nature. 1984;312(5991):275-7. doi: 10.1038/312275a0.
2
Functional modifications of alloreactive T cell clones infected with HTLV-I.感染人嗜T淋巴细胞病毒I型(HTLV-I)的同种反应性T细胞克隆的功能修饰
J Immunol. 1986 Aug 15;137(4):1115-9.
3
Autologous B lymphoblastoid cell lines and long-term cultured T cells as stimulators in the mixed lymphocyte reaction: analysis of the role of HLA class II antigens as stimulatory molecules.自体B淋巴母细胞系和长期培养的T细胞作为混合淋巴细胞反应中的刺激细胞:HLA II类抗原作为刺激分子的作用分析
J Immunol. 1986 Jul 15;137(2):400-7.
4
Characterization of two distinct primary T cell populations that secrete interleukin 2 upon recognition of class I or class II major histocompatibility antigens.两种不同的初始T细胞群体的特征,这两种群体在识别I类或II类主要组织相容性抗原后会分泌白细胞介素2 。
J Exp Med. 1986 Mar 1;163(3):603-19. doi: 10.1084/jem.163.3.603.
5
Requirement of Ia-positive accessory cells in the MLR response against class II antigen on human B cell tumor line.在针对人B细胞肿瘤系上II类抗原的混合淋巴细胞反应中Ia阳性辅助细胞的需求。
J Immunol. 1985 Dec;135(6):3887-96.
6
Cell surface phenotypes and expression of viral antigens of various human cell lines carrying human T-cell leukemia virus.携带人类T细胞白血病病毒的各种人类细胞系的细胞表面表型及病毒抗原表达
Int J Cancer. 1984 Aug 15;34(2):221-8. doi: 10.1002/ijc.2910340213.
7
Human cytotoxic T cell clones directed against herpes simplex virus-infected cells. I. Lysis restricted by HLA class II MB and DR antigens.针对单纯疱疹病毒感染细胞的人细胞毒性T细胞克隆。I. 由HLA II类MB和DR抗原限制的裂解作用
J Immunol. 1984 Jul;133(1):422-7.
8
[Autologous mixed lymphocyte culture (AMLC)].[自体混合淋巴细胞培养(AMLC)]
Allerg Immunol (Leipz). 1984;30(2):60-73.
9
Association of human T-cell leukaemia/lymphoma virus with the Tac antigen marker for the human T-cell growth factor receptor.人类T细胞白血病/淋巴瘤病毒与人类T细胞生长因子受体的Tac抗原标志物的关联。
Nature. 1983;305(5936):733-6. doi: 10.1038/305733a0.
10
Cell surface antigen expression in newborn cord blood lymphocytes infected with HTLV.感染人类嗜T淋巴细胞病毒的新生儿脐带血淋巴细胞中的细胞表面抗原表达
J Immunol. 1983 Oct;131(4):2021-4.

引用本文的文献

1
Mechanisms of T-cell activation by human T-cell lymphotropic virus type I.I型人嗜T细胞病毒激活T细胞的机制
Microbiol Mol Biol Rev. 1999 Jun;63(2):308-33. doi: 10.1128/MMBR.63.2.308-333.1999.
2
Antigenic cross-reactivity between human T lymphotropic virus type I (HTLV-I) and retinal antigens recognized by T cells.人类嗜T淋巴细胞病毒I型(HTLV-I)与T细胞识别的视网膜抗原之间的抗原交叉反应性。
Clin Exp Immunol. 1994 Mar;95(3):459-64. doi: 10.1111/j.1365-2249.1994.tb07019.x.
3
The relationship between HTLV-I-infected cell lines and uveitis.
人类嗜T淋巴细胞病毒I型(HTLV-I)感染的细胞系与葡萄膜炎之间的关系。
Graefes Arch Clin Exp Ophthalmol. 1995 Apr;233(4):231-5. doi: 10.1007/BF00183597.
4
Configuration and expression of the T cell receptor beta chain gene in human T-lymphotrophic virus I-infected cells.人嗜T淋巴细胞病毒I感染细胞中T细胞受体β链基因的构型与表达
J Exp Med. 1986 Feb 1;163(2):383-99. doi: 10.1084/jem.163.2.383.
5
Human T-cell leukemia virus type I infection of CD4+ or CD8+ cytotoxic T-cell clones results in immortalization with retention of antigen specificity.I型人类T细胞白血病病毒感染CD4+或CD8+细胞毒性T细胞克隆会导致永生化,并保留抗原特异性。
J Virol. 1988 Aug;62(8):2942-50. doi: 10.1128/JVI.62.8.2942-2950.1988.
6
HTLV: the family of human T-lymphotropic retroviruses and their role in leukemia and AIDS.人类嗜T淋巴细胞病毒:人类嗜T淋巴细胞逆转录病毒家族及其在白血病和艾滋病中的作用。
Med Oncol Tumor Pharmacother. 1986;3(3-4):265-7. doi: 10.1007/BF02935003.
7
Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures.在受感染的脐血培养物中,前列腺素A可阻止HTLV-I阳性克隆的选择。
Br J Cancer. 1990 Feb;61(2):207-14. doi: 10.1038/bjc.1990.38.
8
Modulation of the cell-mediated immune function by interferon alpha, beta or gamma can partially reverse the immunosuppression induced by human T-cell leukemia virus I in human cord blood cultures.α、β或γ干扰素对细胞介导的免疫功能的调节可部分逆转人类T细胞白血病病毒I在人脐血培养物中诱导的免疫抑制作用。
Cancer Immunol Immunother. 1990;31(4):213-20. doi: 10.1007/BF01789171.
9
Human cervical epithelial cells that express HLA-DR associated with viral infection and activated mononuclear cell infiltrate.表达与病毒感染相关的HLA - DR的人宫颈上皮细胞以及活化的单核细胞浸润。
J Clin Pathol. 1991 Apr;44(4):290-2. doi: 10.1136/jcp.44.4.290.