丙型肝炎病毒核心区多肽对细胞毒T细胞的作用

目的 探讨丙型肝炎病毒（HCV）感染者体内细胞毒T细胞（CTL）功能缺陷的原因。方法 将HCV核心区多肽皮下注射免疫BALB/c小鼠，用乳酸脱氢酶释放实验检测小鼠脾细胞CTL活性，选择上述多肽中对CTL有抑制作用和增强作用的多肽各2条，交叉组合后共同免疫BALB/c小鼠检测其CTL活性。结果 经单因素方差分析显示，HCV核心区多肽CPA9（39-74位氨基酸），CPB7（67-76位氨基酸），CPB8（71-80位氨基酸）对小鼠CTL有抑制作用，CPA10（5-23位氨基酸），CPB6（63-72位氨基酸），CPB2（131-140位氨基酸），对小鼠CTL有增强作用，CPB2 CPB8，CPB6 CPB8组中效靶比10：1，20：1的CTL活性显著高于对照组，CPB2 CPB7，CPB6 CPB7组与对照组无明显差异。双因素方差分析显示HCV核心区抑制性多肽和增强性多肽有交互作用。结论 HCV核心区多肽CPA9，CPB7，CPB8对小鼠CTL有抑制作用。CPA10，CPB6，CPB2对小鼠CTL有增强作用，HCV核心区抑制性和增强性多肽有交互作用。

Effects of polypeptides from HCV core region on the function of cytotoxic T cells

Objective To investigate the pathogenesis of cytotoxic T cell (CTL) dysfunction in patients with HCV infection. Methods BALB/c mice were immunized by subcutaneous injection of polypeptides from HCV core region, and the CTL activity of mouse spleen cells was detected by the LDH release test. Two polypeptides which can enhance CTL function and two polypeptides which can inhibit CTL function were selected and cross-combined. BALB/c mice were immunized using the combined polypeptides and the CTL activities were detected afterwards. Results CTL activity was inhibited by CPA9 (39-74 amino acids), CPB7 (67-76 amino acids) and CPB8 (71-80 amino acids), and promoted by CPA10 (5-23 amino acids), CPB6 (63-72 amino acids) and CPB2 (131-140 amino acids). Using single factor analysis of variance, the CTL activity in the mice could be enhanced by polypeptides from the HCV core region, CPB2+CPB8, CPB6+CPB8, respectively. There was no obvious difference between CPB2+CPB7, CPB6+CPB7 and negative control. Conclusions CPA9, CPB7, and CPB8, the 3 polypeptides from HCV core region play an inhibition role and CPA10, CPB6, and CPB2 play an enhancement role in CTL activity in mice. The inhibition and enhancement functions of the polypeptides from HCV core region interact each other.