Haskins K, Portas M, Bergman B, Lafferty K, Bradley B
Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.
Proc Natl Acad Sci U S A. 1989 Oct;86(20):8000-4. doi: 10.1073/pnas.86.20.8000.
We have produced a panel of islet-specific T-cell clones from nonobese diabetic (NOD) mice. These clones proliferate and make interleukin 2 in an antigen-specific manner in response to NOD antigen-presenting cells and islet cells. Most of the clones respond to islet-cell antigen from different mouse strains but only in the presence of antigen-presenting cells bearing the class II major histocompatibility complex of the NOD mouse. In vivo, the clones mediate the destruction of islet, but not pituitary, grafts. Furthermore, pancreatic sections from a disease transfer experiment with one of the clones showed a pronounced cellular infiltration and degranulation of islets in nondiabetic (CBA x NOD)F1 recipients.
我们从非肥胖型糖尿病(NOD)小鼠中制备了一组胰岛特异性T细胞克隆。这些克隆在响应NOD抗原呈递细胞和胰岛细胞时,以抗原特异性方式增殖并产生白细胞介素2。大多数克隆对来自不同小鼠品系的胰岛细胞抗原有反应,但仅在存在携带NOD小鼠II类主要组织相容性复合体的抗原呈递细胞时才会有反应。在体内,这些克隆介导胰岛移植而非垂体移植的破坏。此外,用其中一个克隆进行疾病转移实验的胰腺切片显示,在非糖尿病(CBA×NOD)F1受体小鼠中,胰岛有明显的细胞浸润和脱颗粒现象。