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目的 探讨抗原特异调节的T细胞在非肥胖型糖尿病 (NOD)小鼠自发性糖尿病中的作用。方法 应用流式细胞计数仪辅以荧光标记组织相容性抗原Ⅱ类分子四聚体染色 ,从自发性糖尿病的NOD小鼠和非糖尿病的BALB/c小鼠中分离出谷氨酸脱羧酶 (GAD)多肽特异性T细胞。分别应用抗原刺激试验、酶联免疫反应、细胞内细胞因子染色检测上述T细胞的细胞因子表达。最后将上述T细胞给NOD/scid小鼠静脉注射 ,检测这些T细胞对糖尿病发生的影响。结果 当用不同多肽诱导同一品系时 ,NOD小鼠T细胞分泌不等量的干扰素 γ ,相似量的白介素 (IL) 4和IL 10 ;BALB/c小鼠T细胞分泌类似量的细胞因子。当同一多肽诱导不同品系时 ,NOD小鼠T细胞较BALB/c小鼠T细胞分泌较少量的IL 2但较大量的IL 4和IL 10。这些NOD小鼠T细胞均可以有效地抑制NOD/scid小鼠的糖尿病发生。结论 两种毗邻的GAD多肽诱导NOD小鼠产生的T细胞表达不同的细胞因子分泌类型 ,但这些NOD小鼠T细胞均可以有效地抑制NOD/scid小鼠的糖尿病 ,因此推论这些细胞为分泌独特细胞因子且抑制糖尿病的T调节细胞。
Objective To investigate the role of antigen-specific T cells in spontaneous diabetes in non-obese diabetic (NOD) mice. Methods Flow cytometry was used in combination with fluorescently labeled histocompatibility antigen class Ⅱ tetramer staining to separate glutamate decarboxylase (GAD) from spontaneous diabetic NOD mice and non-diabetic BALB / c mice ) Polypeptide-specific T cells. Antigen stimulation test, enzyme-linked immunosorbent assay, and intracellular cytokine staining were used to detect the expression of cytokines in these T cells. Finally, the above-mentioned T cells were injected intravenously to NOD / scid mice to examine the effects of these T cells on diabetes. Results When different polypeptides were used to induce the same line, NOD mouse T cells secrete an unequal amount of interferon gamma, similar amounts of interleukin (IL) 4 and IL 10; BALB / c mouse T cells secrete similar amounts of cytokines. NOD mouse T cells secreted less IL 2 but greater IL 4 and IL 10 than BALB / c mouse T cells when the same polypeptide induced different strains. These NOD mouse T cells were able to effectively suppress the onset of diabetes in NOD / scid mice. CONCLUSION: Two adjacent GAD polypeptides induce different cytokine secretion types in T cells derived from NOD mice. However, these NOD mouse T cells can effectively inhibit the diabetes in NOD / scid mice. Therefore, it is concluded that these cells are secreted uniquely Cytokines and T-regulatory cells that inhibit diabetes.