Analysis of the mechanism of autoimmune diseases
Project/Area Number |
17H03612
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Medical genome science
|
Research Institution | University of Tsukuba |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
岡村 匡史 国立研究開発法人国立国際医療研究センター, その他部局等, 実験動物管理室長 (00333790)
|
Project Period (FY) |
2017-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥17,030,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥3,930,000)
Fiscal Year 2019: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2017: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
|
Keywords | HLA / MHC / 1型糖尿病 / 自己免疫疾患 / MHC(主要組織適合性抗原) / ゲノム編集 / 組織適合性抗原(MHC) / ヒト白血球抗原(HLA) |
Outline of Final Research Achievements |
Type 1 diabetes (T1D) occurs through autoimmune-mediated destruction of insulin-producing beta cells in pancreas. The mechanism through which the beta-cells are targeted by self-reactive T-cells have not been fully uncovered. To elucidate the mechanism of T1D, we used non-obese diabetic (NOD) mice, which spontaneously develop T1D, and generated mutant NOD mice that carried mutations in immune molecules. We followed the incidence of T1D for each mutant strain and analyzed immunological responses, to elucidate the relation between immunological function and T1D incidence.
|
Academic Significance and Societal Importance of the Research Achievements |
1型糖尿病の発症は遺伝要因と環境要因の影響を受けるが、免疫応答の変化と自己免疫疾患の罹りやすさとの関係には不明な点が多く残されている。本研究では動物モデルの免疫系分子に変異を導入することにより、免疫分子の機能変化と1型糖尿病発症率との関係について明らかにした。この知見は、1型糖尿病の発症機序の解明につながるものであるだけでなく、他の様々な自己免疫疾患の発症機序の解明と予防法、治療法開発への手がかりを与えるものである。
|
Report
(2 results)
Research Products
(1 results)