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2014 Fiscal Year Final Research Report

Etiology of fulminant type 1 diabetes mellitus

Research Project

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Project/Area Number 24591362
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Endocrinology
Research InstitutionOsaka University

Principal Investigator

IMAGAWA AKIHISA  大阪大学, 医学(系)研究科(研究院), 准教授 (80373108)

Co-Investigator(Renkei-kenkyūsha) HANAFUSA Toshiaki  大阪医科大学, 医学部, 教授 (60164886)
Research Collaborator FUKUI Kenji  
NAKATA Shinsuke  
YOSHIKAWA Atsushi  
HOSOKAWA Yoshiya  
BADEN Megu  
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords1型糖尿病
Outline of Final Research Achievements

The aim of the present study was to determine the significance of ISG15, which is induced by viral infection, and KLRC3, which is known as an activating receptor of NK cells in the development of fulminant type 1 diabetes mellitus.
We found that ISG15 acted as an inhibitor of apoptosis by inflammatory cytokines by using overexpression and knockdown methods in MIN6 cells, mouse beta cell line. We also found that the gene expressions of KLRC3 (NKG2E) and CD94, its heterodimer, were reduced in peripheral NK cells of fulminant type 1 diabetic patients.
Overall, we have clarified two candidates of key molecules in the beta cell destruction of fulminant type 1 diabetes.

Free Research Field

内分泌代謝学

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Published: 2016-06-03  

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