Abstract
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. Key words: Decoy receptor-3; Glutamic acid decarboxylase-65; Diabetes mellitus, experimental; Gene therapy
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