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劳舍尔白血病病毒诱导的肿瘤抗原:与糖蛋白70、p30和H-2完全分离。

Rauscher leukemia virus-induced tumor antigens: complete separation from gp70, p30 and H-2.

作者信息

Alaba O, Rogers M J, Law L W

出版信息

Int J Cancer. 1979 Nov 15;24(5):608-15. doi: 10.1002/ijc.2910240514.

Abstract

The possibility that some or all of the viral proteins, gp70, p30, and the histocompatibility antigen, H-2, function as the tumor-specific transplantation antigen (TSTA) of the R-MuLV-induced leukemia, RBL-5, and also in the secondary in vitro induction of cytotoxic T lymphocytes (CTL), was investigated. The antigen was obtained by isolating the plasma membranes of RBL-5 cells and solubilizing with sodium deoxycholate (DOC) followed by gel filtration chromatography. A fraction containing excellent tumor-rejection activity but low amounts of gp70, p30 and H-2 was chromatographed on goat anti-gp 70 goat anti-p 30 and sheep anti-H-2b immunoaffinity columns. The data obtained indicate that gp 70, p 30 or H-2 do not function as TSTA of RBL-5 leukemia, individually or as a complex. Similarly, the antigen responsible for the specific secondary induction of CTL in vitro is distinct from these three proteins.

摘要

研究了部分或全部病毒蛋白gp70、p30以及组织相容性抗原H-2作为R-MuLV诱导的白血病RBL-5的肿瘤特异性移植抗原(TSTA),以及在体外二次诱导细胞毒性T淋巴细胞(CTL)中的作用可能性。通过分离RBL-5细胞的质膜并用脱氧胆酸钠(DOC)溶解,然后进行凝胶过滤色谱法获得该抗原。将含有优异肿瘤排斥活性但gp70、p30和H-2含量低的部分在山羊抗gp70、山羊抗p30和绵羊抗H-2b免疫亲和柱上进行色谱分析。获得的数据表明,gp70、p30或H-2单独或作为复合物都不作为RBL-5白血病的TSTA。同样,负责体外CTL特异性二次诱导的抗原与这三种蛋白不同。

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