In this thesis, the question is approached whether abnormalities in the islets of Langerhans, in addition to abnormalities in the immune system, are involved in the development of autoimmune diabetes in NOD mice. We found several islet abnormalities, always accompanied by an inflammatory infiltrate. Thus, intrinsic islet abnormalities may indeed play a role in the etiology of NOD autoimmune diabetes. Furthermore, we showed that infiltrating leukocytes can cause islet abnormalities. Thus, a complex cross-talk between antigen-presenting cells and islets exists during development of autoimmune diabetes in NOD mice. A similar interaction may be important in the development of type 1 diabetes in humans.
|Qualification||Doctor of Philosophy|
|Place of Publication||[S.l.]|
|Publication status||Published - 7-Jun-2000|
- Diabetes Mellitus, Type 1