PRIN 2004 - Mechanisms of beta cell damage and prevention strategies of beta cell function in type 1 diabetes - Protocol: 2004063343
Project objectivesType 1 diabetes (DM1) is the most common disease in childhood and adolescence, and can also manifest in adults. Despite recent advances in understanding its pathogenesis, the mechanism responsible for pancreatic beta-cell destruction remains unclear. Immune system alterations have been described in DM1, suggesting that both the induction of immune tolerance and the restoration of lymphocyte balance may promote beta-cell protection and consequently disease prevention. In patients with long-term disease, pancreatic islet cell transplantation may be the definitive therapeutic strategy. In this project, a team of renowned national and international researchers and clinicians specializing in diabetes, from five university institutions and with previous and current collaborations on such projects, will pool their expertise to elucidate some of the mechanisms involved in the pathogenesis of DM1 and to develop new therapeutic strategies. Specific objectives of the project:
The results of this project may shed new light on the pathogenesis of DM1 and offer insights into new treatment strategies both now and in the future. |
Start and end date |
|
30/11/2004 - 10/01/2007 |
Project Manager |
|
Prof. Paolo Pozzilli, Diabetology and Endocrinology Research Unit - Scientific Coordinator of the Research Program |
Coordinating institution of the project |
|
Università Campus Bio-Medico di Roma |
Other Institutions involved |
|
Funding source(s). |
|
Italian Ministry of Education, University and Research |