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在表达小鼠H-2Kb和H-2Db转染基因的猴肾细胞中,在病毒裂解周期期间合成的猿猴病毒40 T抗原被SV40特异性细胞毒性T淋巴细胞识别,导致病毒裂解周期的废除。

Recognition of simian virus 40 T antigen synthesized during viral lytic cycle in monkey kidney cells expressing mouse H-2Kb- and H-2Db-transfected genes by SV40-specific cytotoxic T lymphocytes leads to the abrogation of virus lytic cycle.

作者信息

Bates M P, Jennings S R, Tanaka Y, Tevethia M J, Tevethia S S

机构信息

Department of Microbiology, Pennsylvania State University, College of Medicine, Hershey 17033.

出版信息

Virology. 1988 Jan;162(1):197-205. doi: 10.1016/0042-6822(88)90409-6.

Abstract

Simian virus 40 (SV40)-encoded tumor or T antigen localizes in the membranes in addition to the nucleus of SV40-infected permissive monkey cells and SV40-transformed nonpermissive cells. The surface T antigen in SV40-transformed mouse cells provides a target for the cytotoxic T lymphocytes (CTL) which recognize SV40 T antigen in association with murine K/D, class I H-2 antigens. In order to demonstrate that SV40 T antigen synthesized in SV40-infected permissive monkey kidney cells (TC-7) may also function as a target for CTL, cloned murine H-2Db and H-2Kb genes were expressed in TC-7 cells by DNA transfection and TC-7 cell lines expressing high levels of either H-2Kb or H-Db antigens were established after cell sorting. SV40-infected TC-7/H-2Kb and TC-7/H-2Db cells became susceptible to lysis by SV40-specific H-2b restricted CTL. The susceptibility of these transfected SV40-infected monkey cells to anti-SV40 bulk culture CTL and SV40-specific H-2Db- and H-2Db-restricted CTL clones depended upon the synthesis of SV40 T antigen and the expression of the appropriate H-2Kb or H-2Db restriction elements. Treatment of SV40-infected TC-7/H-2Db and TC-7/H-2Kb with CTL clones abrogated the virus lytic cycle indicating that CTL may play an important role in limiting papovavirus infection in the natural host.

摘要

猿猴病毒40(SV40)编码的肿瘤或T抗原除了定位于被SV40感染的允许性猴细胞和SV40转化的非允许性细胞的细胞核外,还定位于细胞膜。SV40转化的小鼠细胞中的表面T抗原为细胞毒性T淋巴细胞(CTL)提供了一个靶点,这些CTL识别与鼠K/D、I类H-2抗原相关的SV40 T抗原。为了证明在被SV40感染的允许性猴肾细胞(TC-7)中合成的SV40 T抗原也可能作为CTL的靶点,通过DNA转染在TC-7细胞中表达克隆的鼠H-2Db和H-2Kb基因,并在细胞分选后建立了表达高水平H-2Kb或H-Db抗原的TC-7细胞系。被SV40感染的TC-7/H-2Kb和TC-7/H-2Db细胞变得易被SV40特异性H-2b限制性CTL裂解。这些转染的被SV40感染的猴细胞对抗SV40大量培养CTL以及SV40特异性H-2Db和H-2Db限制性CTL克隆的敏感性取决于SV40 T抗原的合成以及适当的H-2Kb或H-2Db限制性元件的表达。用CTL克隆处理被SV40感染的TC-7/H-2Db和TC-7/H-2Kb细胞可消除病毒裂解周期,这表明CTL可能在限制自然宿主中的乳头瘤病毒感染方面发挥重要作用。

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