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以表达人ＣＤ５９ｃＤＮＡ 及ＣＤ５９－ＴＭｃＤＮＡ 的小鼠胸腺瘤（ＥＬ－４）细胞为研究对象，探讨了ＣＤ５９在ｓＭＡＣ诱导ＥＬ－４细胞增殖效应中的作用。结果发现：１）用抗体交联ＣＤ５９分子对ＣＤ５９／ＥＬ－４细胞的增殖有促进效应，而对ＣＤ５９－ＴＭ／ＥＬ－４细胞的增殖无明显影响（Ｐ＜ ０．０１）；２）ｓＭＡＣ对ＣＤ５９／ＥＬ－４细胞的增殖有促进作用，而对ＥＬ－４及ＣＤ５９－ＴＭ／ＥＬ－４细胞则均未出现上述现象（Ｐ＜ ０．０１）；３）阻断信号传导的蛋白酪氨酸激酶途径对上述ＣＤ５９及ｓＭＡＣ介导的ＣＤ５９／ＥＬ－４细胞的增殖有不同的抑制效应。结果提示：ＣＤ５８参与了ｓＭＡＣ诱导ＥＬ－４细胞增殖的效应过程。
To study the effect of CD59 on the proliferation of EL-4 cells induced by sMAC, the mouse thymoma (EL-4) cells expressing human CD59cDNA and CD59-TMcDNA were studied. The results showed that: 1) Anti-CD59 / EL-4 cells were cross-linked with anti-CD59 / EL-4 cells, but had no effect on the proliferation of CD59 / (P <0.01); (3) The signal transduction of the protein cheese (P <0.01) was not observed in EL-4 and CD59-TM / EL-4 cells The kinases pathway has different inhibitory effects on the proliferation of CD59 and sMAC-mediated CD59 / EL-4 cells described above. The results suggest that CD58 is involved in the sMAC-induced proliferation of EL-4 cells.