2002 Fiscal Year Final Research Report Summary
Environmental factor for diabetes, non-insulin-dependent diabetes by virus infection
| Project/Area Number |
13671174
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | Gunma university |
|---|
Principal Investigator |
UTSUGI Toshihiro Gunma University, Second department of Internal Medicine, Assistant Professor, 医学部, 助手 (10282386)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KANDA Tsugiyasu Kanazawa Medical School, Department of General Medicine, Professor, 医学部, 教授 (40261838)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Keywords | Virus-induced diabetes / EMC virus / Mature lymphocyte / islet cells / knockout mouse |
|---|
| Research Abstract |
Virus infection to pancreatic beta cells could be one of environmental factors for the development of diabetes due to dysfunction of pancreatic beta cells. We developed the new animal model for non-insulin dependent diabetes mellitus by infection of the NDK25 variant of encephalomyocarditis (EMC) virus. To study the roles of mature cellular immunity on the pathogenesis of this model, RAG-2 knockout (KO) mice were infected with the NDK25 variant of EMCV. The original strain, 129/SvEv mouse was used as control. Glucose intolerance was observed in RAG-2KO, but not in control. Histological study showed that the pancreatic islets were mildly destroyed and the virus genome was detected in the islets in RAG-2KO, whereas the pancreatic islets appeared normal in control. Secondly, to elucidate roles of each lymphocyte subset in this model, MHC class II deficient mice, MHC class I deficient mice, and B-cell deficient mice, were infected with the NDK25 of EMCV. No mice showed glucose intolerance, and histological study demonstrated normal appearance of pancreatic islets in these mice.
From these results, we conclude that mature cellular immunity play a protective role against viral infection on the pathogenesis of glucose intolerance, and, once infected, the destruction of pancreatic beta cells by EMCV depends on their own ability to destroy beta cells
|
