The crosstalk between SR-A and TLR4 on dendritic cells influences the development of type 1 diabetes.

2016 Fiscal Year Final Research Report

• Project/Area Number: 15H06403
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: General internal medicine(including psychosomatic medicine)
• Research Institution: Kobe University
• Principal Investigator: Shimizu Mami 神戸大学, 医学研究科, 医学研究員 (10757313)
• Research Collaborator: INOUE Yuto 神戸大学, 大学院保健学研究科 ; WAKAFUJI Ryo 神戸大学, 大学院保健学研究科 ; TAGAMI Kanako 神戸大学, 大学院保健学研究科 ; NISHIKAWA Minaho 神戸大学, 大学院保健学研究科 ; KATSUTA Atsumi 神戸大学, 大学院医学研究科, 研究助手
• Project Period (FY): 2015-08-28 – 2017-03-31
• Keywords: １型糖尿病 / SR-A / 腸内細菌 / ＴＬＲ４

Outline of Final Research Achievements

Recently, it has been reported that the development of type 1 diabetes would be associated with commensal bacteria. So the aim of this study was to examine the association between scavenger receptor A (SR-A) and Toll-like receptor 4 (TLR4) as a sensor of the gram-negative rod on dendritic cells and to establish a new immunological preventative and therapeutic strategy for type 1 diabetes. First, lipopolysaccharide (LPS) as a ligand of TLR4 was administered to female NOD mice and cyclophosphamide (CY) -induced diabetes model in male NOD mice. Second, LPS was administered to SR-A KO NOD mice and CY-induced diabetes model in SR-A KO NOD mice. As a result, LPS administration prevented diabetes onset in female NOD mice and CY-induce diabetes model in male NOD mice, but not in SR-A KO situations. Flow cytometric analysis suggested that the Foxp3 regulatory T cells might play a pivotal role in the mechanism of LPS tolerance.

Free Research Field

1型糖尿病