PROGRESSION FROM INSULITIS TO BETA-CELL DESTRUCTION IN NOD MOUSE REQUIRES L3T4+ LYMPHOCYTES-T
PROGRESSION FROM INSULITIS TO BETA-CELL DESTRUCTION IN NOD MOUSE REQUIRES L3T4+ LYMPHOCYTES-T
复制标题
DOI：
10.2337/diabetes.37.8.1108
复制
发表时间：
1988-08-01
期刊：
影响因子：
7.7
通讯作者：
MANDEL, TE
中科院分区：
文献类型：
--
作者：
CHARLTON, B;MANDEL, TE
负责β的细胞的身份- I型（胰岛素依赖型）糖尿病中的细胞破坏仍不确定。L3 T4 + T淋巴细胞在非肥胖糖尿病（NOD）小鼠胰岛炎的起始和移植的同种异体胰岛损伤中起作用。L3 T4 + T-淋巴细胞在β-T细胞破坏中的作用用大鼠抗L3 T4单克隆抗体（MoAb）在环磷酰胺（CY）诱导的糖尿病NOD小鼠中研究NOD小鼠的细胞。在施用CY后，大多数未治疗的动物变成糖尿病，而所有抗体治疗的动物保持血糖正常。胰岛炎仍然存在于单克隆抗体治疗的动物，但免疫细胞化学染色显示大鼠抗体阻断T淋巴细胞上的L3 T4抗原。该研究提供了L3 T4 + T-淋巴细胞对β-CD过程至关重要的进一步证据。NOD小鼠中的细胞破坏。L3 T4+细胞发挥其作用的方式仍有待澄清。
The identity of the cells responsible for .beta.-cell destruction in type I (insulin-dependent) diabetes is still uncertain. L3T4+ T-lymphocytes have a role in the initiation of insulitis and in damaging transplanted allogeneic islets in nonobese diabetic (NOD) mice. The role of L3T4+ T-lymphocytes in destruction of .beta.-cells of the NOD mouse was studied in cyclophosphamide (CY)-induced diabetic NOD mice with a rat anti-L3T4 monoclonal antibody (MoAb). After administration of CY, most untreated animals became diabetic, whereas all antibody-treated animals remained normoglycemic. Insulitis was still present in MoAb-treated animals, but immunocytochemical staining showed rat antibody blocking the L3T4 antigen on T-lymphocytes. This study provides further evidence that L3T4+ T-lymphocytes are critical to the process of .beta.-cell destruction in NOD mice. The means by which L3T4+ cells exert their effect remains to be clarified.