| Project/Area Number |
13140203
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
|
| Allocation Type | Single-year Grants |
|---|
| Review Section |
Biological Sciences
|
|---|
| Research Institution | Kyoto University |
|---|
Principal Investigator |
SAKAGUCHI Shimon Kyoto University Institute for Frontier Medical Sciences, Professor, 再生医科学研究所, 教授 (30280770)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
INABA Kayo Grad Schl. Biostudies, Dept. Animal Develop. Physiology, Professor, 生命科学研究科, 教授 (00115792)
KIKUTANI Hitoshi Osaka University Research Institute for Microbial Diseases, Professor, 微生物研究所・分子免疫制御分野, 教授 (80161412)
AZUYMA Miyuki Tokyo Medical and Dental University Department molecular, Immunology Professor, 大学院医歯学総合研究科, 教授 (90255654)
HIROSE Sachiko Juntendo University School of Medcine, AssociateProfessor, 医学部, 助教授 (00127127)
中野 直子 東京理科大学, 生命科学研究所, 助教授 (90222166)
高橋 武司 京都大学, 再生医科学研究所, 助手 (80335215)
|
|---|
| Project Period (FY) |
2001 – 2006
|
| Project Status |
Completed (Fiscal Year 2006)
|
| Budget Amount *help |
¥155,500,000 (Direct Cost: ¥155,500,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥31,500,000 (Direct Cost: ¥31,500,000)
Fiscal Year 2004: ¥31,500,000 (Direct Cost: ¥31,500,000)
Fiscal Year 2003: ¥31,500,000 (Direct Cost: ¥31,500,000)
Fiscal Year 2002: ¥31,500,000 (Direct Cost: ¥31,500,000)
Fiscal Year 2001: ¥28,000,000 (Direct Cost: ¥28,000,000)
|
|---|
| Keywords | Autoimmune disease / Regulatory T cell / Dendritic cells / Semaphoring / Co-stimulatory molecule / Genetic susceptibilit / Immunological self-tolerance / Foxp3 / 自己免疫 / 腫瘍免疫 / 移植免疫 / GITR-L / Gpr83 / helios / CD25 / 単クローン抗体 / 病理学 / 免疫学 / GITR / CTLA-4 |
|---|
| Research Abstract |
The aim of this project is to elucidate the cause and the pathogenetic mechanism of autoimmune disease, and seek for effective ways of its treatment and prevention. Five researchers as principal investigators of the project conducted the following research. Shimon Sakaguchi studied the molecular and cellular basis of natural regulatory T cells and found that the transcription factor Foxp3 is a master control molecule for the development and function of regulatory T cells. Transduction of Foxp3 into normal T cells was indeed able to convert them to regulatory T cells functionally in humans and mice. Kayo Inaba showed that dendritic cells, which are a potent activator of T cell immune responses, also play a key role in induction and expansion of regulatory T cells when dendritic cells become mature. Hitoshi Kikutani characterized CD40, several semaphorin molecules, and their respective ligands, and showed their roles in controlling immune responses. He produced monoclonal antibodies specific for some of semaphoring molecules and showed that the antibodies could suppress the development of autoimmune disease in mouse models. Miyuki Azuma studied the roles of co-stimulatory molecules, in particular PD1, ICOS and GITR?, for T cell activation, and attempted to treat autoimmune disease in mouse models by raising monoclonal antibodies specific for these molecules. Sachiko Hirose conducted genetic study to identify and characterize the susceptibility genes for systemic autoimmune disease. She showed that the polymorphism of the LTK, FcgRIIB and other genes in a lupus model mouse, and confirmed the LTK polymorphism in human lupus as well.
|
