Chong Anita S, Shen Jikun, Tao Jing, Yin Dengping, Kuznetsov Andrey, Hara Manami, Philipson Louis H
Section of Transplantation, Department of Surgery, University of Chicago, Chicago, IL 60637, USA.
Science. 2006 Mar 24;311(5768):1774-5. doi: 10.1126/science.1123510.
Autoimmune destruction of beta cells is the predominant cause of type 1 diabetes mellitus (T1DM) in humans and is modeled in non-obese diabetic (NOD) mice. Many therapeutic interventions prevent the development of T1DM in NOD mice, but few can induce its reversal once established. Intervention with Freund's complete adjuvant, semi-allogeneic splenocytes, and temporary islet transplantation has been reported to cure NOD mice of established T1DM. Using the same approach, we report here that this treatment cured 32% of NOD mice of established diabetes (>340 milligrams per deciliter blood glucose), although beta cells in these mice were not derived from donor splenocytes.
β细胞的自身免疫性破坏是人类1型糖尿病（T1DM）的主要病因，非肥胖糖尿病（NOD）小鼠可作为该疾病的模型。许多治疗干预措施可预防NOD小鼠发生T1DM，但一旦疾病确立，很少有干预措施能诱导其逆转。据报道，使用弗氏完全佐剂、半同种异体脾细胞和临时胰岛移植进行干预可治愈已患T1DM的NOD小鼠。采用相同方法，我们在此报告，这种治疗治愈了32%已患糖尿病（血糖>340毫克/分升）的NOD小鼠，尽管这些小鼠的β细胞并非来源于供体脾细胞。
