诱骗受体3和谷氨酸脱羧酶65重组腺病毒对糖尿病小鼠的作用研究

Effect of decoy receptor-3 and glutamic acid decarboxylase-65 recombinant adenovirus on type 1 diabetes mice

构建诱骗受体3（DcR3）和谷氨酸脱羧酶65（ GAD65）重组腺病毒载体,转染树突状细胞,干预1型糖尿病小鼠,观察小鼠体内CD＋8T细胞的活化抑制情况和血糖水平.结果显示转染重组腺病毒的树突状细胞能有效抑制GAD65特异性T细胞的增殖和细胞因子的分泌,γ-干扰素[（50.5±7.2）对（95.4±6.9）、（91.2±6.5）pg/ml]和白细胞介素2[（46.3±5.1）对（86.1±5.2）、（80.3±7.3） pg/ml]低于阴性和空白对照组（均P＜0.05）,同时延缓1型糖尿病的发生.提示DcR3和GAD65重组腺病毒可用于1型糖尿病的基因治疗.

The decoy receptor-3 （ DcR3 ） and glutamic acid decarboxylase-65 （ GAD65 ） recombinant adenovirus was construced and transduced into denlritic cells （DC）. After the transduced DC were utilized to immunize NOD mice,the CD＋8 T cells and blood glucose were analyzed. The results showed that recombinant adenovirus inhibited the proliferation and cytokine release of GAD65 specific T cells,and delayed the incidence of diabetes.Both interferon-γ[ （50.5±7.2）vs（95.4±6.9） and（91.2±6.5） pg/ml] and interleukin-2 [ （46.3±5.1 ）vs （ 86.1 ±5.2 ） and （ 80.3 ± 7.3 ） pg/ml ] were decreased compared to those in negative and blank controls （ all P〈0.05 ）.The results suggest that DcR3 and GAD65 recombinant adenovirus might provide a promising way for gene therapy of type 1 diabetes.