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MHC-I类分子在诱导肿瘤浸润淋巴细胞细胞毒活性中的作用 被引量:12

THEROLEOFMHC-1MOLECULESININDUCTIONOFSECIFICCYTOTOXICACTIVITYOFTILs
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摘要 选用H_22(小鼠肝癌)、B_16(小鼠黑色素瘤)和E_(10)(小鼠淋巴瘤)三种动物模型分离肿瘤浸润淋巴细胞(TumorinfiltratingLymphocytes,TILs),在含IL-2200U/ml的培养系统中以60钴灭活自身瘤细胞,周期性刺激进行扩增。实验发现,被选用的三种动物瘤株中。仅从E_(10)淋巴瘤分离的TIL显示明显的增殖和对自身瘤细胞的杀伤活性。对三种瘤株体外MHC限制性观察结果表明,未测出H_(22)、B_(16)瘤株细胞表达K ̄b、D ̄b、K ̄k、D ̄k、K ̄d、D ̄d位点编码的MHC-I类分子,而E_(10)瘤细胞则表达强阳性的K ̄b、D ̄b位点编码的MHC-I类分子。此外,H_(22)、B_(16)瘤细胞可在多种品系(C_(57)BL/6、C_3H、Balb/C及昆明种)小鼠中生长,而E_(10)瘤株只限制在C_(57)BL/6品系小鼠中生长。 _(22)(Hepatoma),B_(16)(Melanoma)and E_(10)(Lymphoma)were used to separate tumor infiltrat-ing lymphocytes(TILs). TILs were cultured in RPMI1640 Medium Containing IL-200U/mland periodically stimulated with inactivated autologous tumor cells.TILs with specific cytotoxici- ty from E_(10)(lymphoma) but not H_(22)、B_(16) could be induced successfully.Experiments in whichH_(22)、B_(16) and E_(10) tumor cells were separately innoculated subcutaneously in several strains of mice(C_(57)BL/6、 C_3H、Balb/C and Kun-ming strain)showed that both H_(22) and B_(16)tumor cells(couldgrow in all strains of mice,but E_(10) tumor was seen only in C_(57)BL/6mice. Using one-way mixedlymphocyte reaction to induce allo-specific cytotoxic T cells,we found that allo-specific CTLs a- gainst H-2 ̄b haplotype could kill the E_(10) but not the B_(16) cells, Again, the allo-specific CTL againstH-2 ̄k haplotype showed no cytotoxicity to H_(22)tumor cells.Furthermore.Using antiH-2K. D spe-cific typing serum to detect the expression of MHC-1molecules on the surface of tumor cells,wefound that MHC-1molecules could not be detected on the surface of H_(22)and B_(16) tumor cells butdetected on E_(10)lymphoma cells.This implied that tumor cells without expression or only withlow expression of MHC-1molecules could not be used to induce the specific cytotoxicity of tu- mor infiltrating lymphocytes.
出处 《中国免疫学杂志》 CAS CSCD 北大核心 1994年第4期195-198,共4页 Chinese Journal of Immunology
关键词 肿瘤浸润 淋巴细胞 MHC Tumor-infiltrating lymphocytes TILs MHC-1 molecules Allo-specific CTL
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