CAJ | 학술논문

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.
구건유편수체3(DcR3)화곡안산탈최매65( GAD65)중조선병독재체,전염수돌상세포,간예1형당뇨병소서,관찰소서체내CD+8T세포적활화억제정황화혈당수평.결과현시전염중조선병독적수돌상세포능유효억제GAD65특이성T세포적증식화세포인자적분비,γ-간우소[(50.5±7.2)대(95.4±6.9)、(91.2±6.5)pg/ml]화백세포개소2[(46.3±5.1)대(86.1±5.2)、(80.3±7.3) pg/ml]저우음성화공백대조조(균P＜0.05),동시연완1형당뇨병적발생.제시DcR3화GAD65중조선병독가용우1형당뇨병적기인치료.
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.