2007 Fiscal Year Final Research Report Summary
Contribution of NK cells and NK related molecules in autoimmunity
| Project/Area Number |
18590484
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Research Institute, International Medical Center of Japan |
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Principal Investigator |
OGASAWARA Kouetsu Research Institute, International Medical Center of Japan, The Research Institute Department of Intractable Diseases, Division of Clinical Immunnology, Head (30323603)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Naruyoshi The Research Institute, International Medical Center of Japan, Department of Intractable Diseases, Division of Clinical Immunnology, Fellow (50365425)
TANAKA Kazusa (ISHIZAKI, Kazusa) The Research Institute, International Medical Center of Japan, Department of Intractable Diseases, Division of Clinical Immunnology, Fellow
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| Project Period (FY) |
2006 – 2007
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| Keywords | autoimmunity / NKG2D / Diabetes / NODマウス / RAE-1 |
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| Research Abstract |
Autoimmune diseases are caused by abnormal immune responses in self-tissues. Co-stimulatory molecules play important roles in immune responses. We focused the signaling mechanisms of co-stimulatory molecules and their ligands to explore development of autoimmune diseases. Type I diabetes is an autoimmune disease in which insulin-producing beta cells in pancreatic islets are destroyed by auto-reactive T cells. We showed that autoreactive T cells infiltrating the pancreas in diabetic NOD mice express NKG2D and NKG2D ligands are present in the pre-diabetic pancreas islets. Treatment with anti-NKG2D monoclonal antibody during the pre-diabetic stage completely prevented disease by impairing expansion of autoreactive T cells and blocking their effector functions. However, the molecular mechanisms by which RAE-1, one of NKG2D ligands are expressed in the pancreas in the development diabetes are unknown. We found that RAE-1 expression is regulated by transcriptional factors and that RAE-1 alpha is a major NKG2D ligand in NOD. In addition, transcriptional activator (s) derived from NOD may regulate RAE-1 alpha expression.
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[Journal Article] A novel avian homologue of CD72, chB1r, down modulates BCR-mediated activation signals.2006
Author(s)
Fujiwara N, Hidano S, Mamada H, Ogasawara K, Kitamura D, Cooper MD, Hozumi N, Chen CL, Goitsuka R
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Journal Title
Int Immunol 18(5)
Pages: 775-83
Description
「研究成果報告書概要(欧文)」より
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