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ＮＯＤ鼠是人类胰岛素依赖型糖尿病的动物模型，其发病与自身免疫有关。环磷酰胺（ＣＰ）可以加速这一过程，使ＮＯＤ鼠糖尿病的发病率提高或提前。一些研究表明：ＮＯＤ鼠的淋巴细胞在淋巴细胞混合反应中（ＭＬＲ），在有或无刺激物的存在下，白细胞介素２（ＩＬ－２）的产量均明显低于正常鼠的淋巴细胞。该实验对注射了一次大剂量的ＣＰ（３００ｍｇ／ｋｇ体重）后的ＮＯＤ鼠试用了ＩＬ－２治疗。结果显示：对于年幼的ＮＯＤ鼠ＩＬ－２治疗１４无可以明显减轻注射ＣＰ后的胰岛破坏加速。病理检查显示三组胰岛炎严重程度积分分别为２９；８１；８８。ＩＬ－２处理组明显低于ＣｏｎＡ处理组与对照组。这个研究还显示，对于１２周龄的ＮＯＤ鼠，经１４天的ＩＬ－２治疗，可以完全预防ＣＰ诱导的糖尿病的发生。糖尿病发病率在ＩＬ－２组为０／１２；对照组为７／１２。但对已发病的ＮＯＤ鼠自发性糖尿病ＩＬ－２不能使其缓解。
NOD mice are an animal model of human insulin-dependent diabetes mellitus, whose pathogenesis is related to autoimmunity. Cyclophosphamide (CP) accelerates this process, increasing or increasing the incidence of diabetes in NOD mice. Some studies have shown that the production of interleukin 2 (IL-2) in lymphocytes of NOD mice was significantly lower than that of normal mice in the mixed lymphocyte reaction (MLR) in the presence or absence of stimuli. In this experiment, NOD mice injected with a large dose of CP (300 mg / kg body weight) were treated with IL-2. The results showed that IL-2 treatment 14 in young NOD mice did not significantly reduce the accelerated islet destruction after injection of CP. Pathological examination showed that the severity of insulitis in the three groups was 29; 81; 88, respectively. IL-2 treatment group was significantly lower than ConA treatment group and control group. This study also showed that for 12-week-old NOD mice, CP-induced diabetes was completely prevented by 14 days of IL-2 treatment. The incidence of diabetes was 0/12 in the IL-2 group and 7/12 in the control group. However, spontaneous IL-2 in spontaneously diabetic NOD mice has not been alleviated.