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2019 Fiscal Year Final Research Report

High-order mechanism for regulating immune function of macrophages using a new recombinant protein and its clinical application

Research Project

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Project/Area Number 17K08999
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Laboratory medicine
Research InstitutionNagahama Institute of Bio-Science and Technology

Principal Investigator

Ikemoto Masaki  長浜バイオ大学, バイオサイエンス学部, 客員教授 (80144385)

Co-Investigator(Kenkyū-buntansha) 伊藤 洋志  長浜バイオ大学, バイオサイエンス学部, 准教授 (20362387)
岡田 光貴  京都橘大学, 健康科学部, 助教C (80747569)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywordsマクロファージ / 炎症性サイトカイン / 間質性肺炎 / 強皮症 / 組換えタンパク質 / 難病 / 免疫複合体
Outline of Final Research Achievements

Recombinant human MIKO-1 and its derivatives (-1a, -1b, -1c) were newly developed by gene technology. hMIKO-1 strongly suppressed the onset of experimental colitis induced with 5% DSS in rats. hMIKO-1 intracellularly entered into macrophages and further migrated inside their nucleus. It was strongly suggested that hMIKO-1 could inhibit the pathway of NF-kappa B by negatively regulating the expression of inflammatory cytokines's mRNAs.
On the other hand, we confirmed that hMIKO-1 also entered into macrophages and further migrated inside the nucleus. It was also noteworthy that hMIKO-1 strongly suppressed the onset of indirect pneumonia and systemic sclerosis in mouse.

Free Research Field

臨床生化学,臨床免疫学

Academic Significance and Societal Importance of the Research Achievements

hMIKO-1は核内における炎症性サイトカインmRNAの発現を強く阻害すること,細胞質で産生された炎症性サイトカインを細胞質内で複合体を形成することにより,炎症誘導過程を阻害すると考えられる.これはToll-like recptor 4を介する経路を阻害している可能性が高いことから,潰瘍性大腸炎だけでなくマクロファージの異常活性化を原因とする他の炎症性疾患に対しても有効と考えられる.事実,間質性肺炎や強皮症においてもその有効性が確認された.これらの成果は難病の原因解明に貢献でき,その社会的意義は大変大きい.また,hMIKO-1のアミノ酸配列の解析は新しいタンパク質科学の発展に寄与できる.

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Published: 2021-02-19  

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