Balasa B, Boehm B O, Fortnagel A, Karges W, Van Gunst K, Jung N, Camacho S A, Webb S R, Sarvetnick N
Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
Clin Immunol. 2001 May;99(2):241-52. doi: 10.1006/clim.2001.5012.
The nonobese diabetic (NOD) mouse develops spontaneous T-cell-dependent autoimmune diabetes. We tested here whether vaccination of NOD mice with a plasmid DNA encoding glutamic acid decarboxylase (GAD), an initial target islet antigen of autoimmune T cell repertoire, would modulate their diabetes. Our results showed that vaccination of young or old female NOD mice with the GAD-plasmid DNA, but not control-plasmid DNA, effectively prevented their diabetes, demonstrating that GAD-plasmid DNA vaccination is quite effective in abrogating diabetes even after the development of insulitis. The prevention of diabetes did not follow the induction of immunoregulatory Th2 cells but was dependent upon CD28/B7 costimulation. Our results suggest a potential for treating spontaneous autoimmune diabetes via DNA vaccination with plasmids encoding self-Ag.
非肥胖糖尿病（NOD）小鼠会自发发展出T细胞依赖性自身免疫性糖尿病。我们在此测试了用编码谷氨酸脱羧酶（GAD，自身免疫性T细胞库的初始靶胰岛抗原）的质粒DNA对NOD小鼠进行疫苗接种是否会调节其糖尿病。我们的结果表明，用GAD质粒DNA而非对照质粒DNA对年轻或年老雌性NOD小鼠进行疫苗接种可有效预防其糖尿病，这表明即使在胰岛炎发展后，GAD质粒DNA疫苗接种在消除糖尿病方面也相当有效。糖尿病的预防并非遵循免疫调节性Th2细胞的诱导，而是依赖于CD28/B7共刺激。我们的结果表明，通过用编码自身抗原的质粒进行DNA疫苗接种来治疗自发性自身免疫性糖尿病具有潜力。
