膜表达型InsB_(15-23) H-2K^d dtSCT对NOD小鼠1型糖尿病发病的影响

Membrane-expressed InsB_(15-23) H-2K^d dtSCT can reduce morbidity of type 1 diabetes mellitus in NOD mice

目的:研究膜表达型Ins B15-23H-2Kddt SCT对NOD小鼠1型糖尿病发病率的影响。方法:用Ins B15-23mdt SCT真核表达载体皮下免疫3周龄NOD母鼠,连续监测NOD小鼠的血糖水平以判断小鼠的发病情况。通过连续切片对NOD小鼠胰岛单个核细胞浸润情况进行检测,并监测IGRP206-214特异性CTLs的变化,来阐明Ins B15-23mdt SCT分子影响1型糖尿病病程的细胞学机制。结果:Ins B15-23mdt SCT组小鼠30周龄时的发病率(9%)显著低于空质粒组(60%)和自然发病组(80%),胰岛单个核细胞浸润情况也较轻,但16和40周龄时两组小鼠外周血IGRP206-214特异性CTLs水平无差异。结论:Ins B15-23mdt SCT真核表达载体能降低NOD小鼠1型糖尿病发病率,并且这种免疫保护作用是IGRP206-214非依赖性的。

Objective： To illuminate the influence of Ins B15-23H-2K^ddt SCT to the morbidity of type 1 diabetes mellitus in NOD mice. Methods： An eukaryotic plasmid encoded membrane-expressed Ins B15-23H-2K^ddt SCT was inoculated into 3 weeks old female NOD mice subcutaneously and the blood sugar and morbidity of type 1 diabetes mellitus were monitored once a week. To illuminate the cellular mechanism of immunologic intervention of membrane-expressed Ins B15-23H-2K^ddt SCT to the course of type 1 diabetes mellitus in NOD mice,the mononuclear cell infiltration of islets was detected by tissue slice and the frequency of IGRP206-214 specific CTLs in PBMC was analyzed by FACs. Results： As compared with pc DNA3. 1（-） control（ 60%） and untreated NOD mice（ 80%）,mice immunized with Ins B15-23H-2K^ddt SCT exhibited low level of islet infiltration and low morbidity in 30 weeks old（ 9%）. But the frequency of IGRP206-214 specific CTLs in PBMC of 16 and 40 weeks old mice showed no difference. Conclusion： Membrane-expressed Ins B15-23H-2Kddt SCT can protect NOD mice from type 1 diabetes mellitus in IGRP206-214 independent pattern.