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Abstract
目的：观察融合蛋白胞质转导肽（cytoplasmic transduction peptide,CTP）-HBcAg_（18-27）-Tapasin通过介导JAK/STAT通路诱导近交系C57BL/6小鼠HBV特异性细胞毒性T淋巴细胞（cytotoxic T lymphocyte,CTL）反应.方法：C57BL/6小鼠随机分为4组：CTPHBcAg_（18-27）-Tapasin实验组、CTP-HBcAg_（18-27）-Tapasin＋AG490对照组、AG490对照组、PBS空白组.融合蛋白经肌肉注射免疫小鼠,腹腔注射AG490阻断JAK/STAT通路,CCK-8比色法检测T淋巴细胞增殖活性;流式细胞术检测T淋巴细胞内的的细胞因子;ELISA检测T淋巴细胞分泌细胞因子,Real-time PCR检测JAK/STAT通路信号分子表达水平.结果：CTP-HBcAg_（18-27）-Tapasin组相比CTPHBcAg_（18-27）-Tapasin＋AG490组CD8~＋IFN-γ~＋T双阳性细胞百分比显著增加（P〈0.01）,淋巴细胞增殖活性差异具有显著性（P〈0.01）,Th1型细胞因子分泌水平显著增加（P〈0.01）,其他各组之间没有显著性差异,JAK/STAT信号通路信号中Jak2,STAT4 mRNA分子表达水平CTP-HBcAg_（18-27）-Tapasin组相比其他对照组表达水平差异具有显著性（P〈0.05）,CTP-HBcAg_（18-27）-Tapasin组Tyk2、STAT1mRNA的分子表达水平相比其他对照组表达水平具有显著性差异（P〈0.01）.结论：本研究表明CTP-HBcAg_（18-27）-Tapasin通过JAK/STAT信号通路促进Th1型细胞因子的分泌而促进特异性CTL反应.
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