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同基因H-2基因的转染和表达不会降低H-2阴性畸胎瘤细胞在自体宿主中的恶性程度。

Transfection and expression of syngeneic H-2 genes does not reduce malignancy of H-2 negative teratocarcinoma cells in the autologous host.

作者信息

Ostrand-Rosenberg S, Cole G A, Nishimura M I, Clements V K

机构信息

Department of Biological Sciences, University of Maryland Baltimore County 21228.

出版信息

Cell Immunol. 1990 Jun;128(1):152-64. doi: 10.1016/0008-8749(90)90014-i.

Abstract

Rejection of the MHC class I negative 402AX teratocarcinoma is accompanied by induction of tumor cell-encoded H-2K and H-2D antigens by the genetically resistant host. To determine whether MHC antigen expression is required for 402AX rejection, we have prepared H-2Db-transfected 402AX cells (402AX/Db). Transfectants express high levels of H-2Db, most of which is not associated with beta 2-microglobulin. MHC syngeneic and allogeneic mice susceptible to 402AX are resistant to 402AX/Db, suggesting that MHC class I antigen expression is required for tumor rejection. Autologous 129 hosts, however, are susceptible to 402AX/Db. 402AX cells transfected with the H-2Kb gene (402AX/Kb) are also lethal in the autologous 129/J host, but rejected by MHC syngeneic and allogeneic mice. Non-129 strain 402AX-susceptible mice pre-immunized with 402AX/Db or simultaneously challenged with 402AX/Db plus 402AX are immune to 402AX. Mice immunized with 402AX/Db produce MHC class I induction factor. 402AX/Db and 402AX cells are lysed equally by natural killer cells, indicating that in 402AX cells the expression of class I antigens is unrelated to NK susceptibility. These studies confirm the requirement for class I expression in 402AX immunity, but demonstrate that in the autologous host immunity requires additional factors beyond class I antigen expression.

摘要

对MHC I类阴性的402AX畸胎癌的排斥反应伴随着遗传抗性宿主诱导肿瘤细胞编码的H-2K和H-2D抗原。为了确定402AX排斥反应是否需要MHC抗原表达,我们制备了转染H-2Db的402AX细胞(402AX/Db)。转染细胞表达高水平的H-2Db,其中大部分与β2-微球蛋白不相关。对402AX敏感的MHC同基因和异基因小鼠对402AX/Db有抗性,这表明肿瘤排斥反应需要MHC I类抗原表达。然而,自体的129宿主对402AX/Db敏感。用H-2Kb基因转染的402AX细胞(402AX/Kb)在自体129/J宿主中也是致死性的,但被MHC同基因和异基因小鼠排斥。预先用402AX/Db免疫或同时用402AX/Db加402AX攻击的非129品系402AX敏感小鼠对402AX免疫。用402AX/Db免疫的小鼠产生MHC I类诱导因子。402AX/Db和402AX细胞被自然杀伤细胞同等程度地裂解,这表明在402AX细胞中I类抗原的表达与NK敏感性无关。这些研究证实了402AX免疫中I类表达的必要性,但表明在自体宿主中免疫需要I类抗原表达之外的其他因素。

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