Gene therapy for autoimmune diabetes by DNA vaccine

DNA疫苗对自身免疫性糖尿病基因治疗的研究综述如下。(1) th1主导的全身免疫反应参与自身免疫性胰岛素的发展，可能通过il -12诱导和il -18激活的机制诱导。(2)层粘连蛋白的表达与NZBxNZWf1小鼠颌下腺的细胞浸润有关。(3) C57BL/6小鼠支气管病变的减少至少部分是由于抑制Th2免疫反应，Th2免疫反应是导致淋巴细胞和嗜酸性粒细胞浸润支气管粘膜减少的基础。(4) NZBxNZWF1小鼠血清IFN-r升高可能与活动性疾病相关。(5)哺乳小鼠感染Reo-2引起的胰岛素炎是由免疫反应引起的。(6)系统给药ifn -r表达质粒可能具有调节Th1/Th2平衡的能力，通过Th1和Th2细胞间的相互抑制机制下调Th2应答，导致LAR降低。(7) IFN-r参与了NZBxNZWF1小鼠狼疮的发展，而IL-4没有参与。(8) ifn -r编码质粒促进reo -2诱导糖尿病的自身免疫性胰岛素。(9) CpG ODN可能通过Th1细胞因子特别是IFN-r的附加作用，促进reo -2诱导的针对胰岛细胞的自身免疫反应。（10） ICAM-1/LFA-1可能是由Th0细胞向Th1细胞分化所必需的，而Th1细胞介导了reo -2感染的哺乳小鼠的胰岛素炎症。

Summary consisted of 10 items listed bellow concerning gene therapy for autoimmune diabetes by DNA vaccine. (1)Th1-dominant systemic immune responses, being responsible for the development of autoimmune insulitis, might be induced by IL-12-induced and IL-18-activated mechanisms. (2)Laminin expression is associated with the cellular infiltration of the submandibular salivary gland of NZBxNZWf1 mice. (3) The reduced bronchial lesions in C57BL/6 mice were due, at least in part, to suppression of the Th2 immune response that underlies the decreased infiltration of lymphocytes and eosinophils into the bronchial mucosa. (4) Increase in serum IFN-r may be associated with the active disease in NZBxNZWF1 mice. (5) The insulitis seen in Reo-2 infection in suckling mice is induced by an immune reaction. (6) The systemic administration of IFN-r-expressing plasmid may have a modulating ability of Th1/Th2 balance to down-regulate Th2 response by mutual inhibitoru mechanisms between Th1 and Th2 cells, leading to the reduction of th LAR. (7) IFN-r but not IL-4 contribute to the development of lupus in the NZBxNZWF1 mice. (8) The IFN-r-encoding plasmid promoted autoimmune insulitis in Reo-2-induced diabetes. (9) CpG ODN may contribute to accelerate Reo-2-induced autoimmune reaction against pancreatic islet cells via additional effects of Th1 cytokine especially IFN-r. (10) ICAM-1/LFA-1 may be required for the differentiation of Th0 cells to Th1 cells, which mediate insulitis with IGT in Reo-2-infected suckling mice.