Elucidation of the protective mechanism of dendritic cells regulated by TRAF6 signaling against Dengue virus infection

2016 Fiscal Year Final Research Report

• Project/Area Number: 15H06512
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Pathobiological dentistry/Dental radiology
• Research Institution: Oita University
• Principal Investigator: Kamiyama Naganori 大分大学, 医学部, 助教 (50756830)
• Project Period (FY): 2015-08-28 – 2017-03-31
• Keywords: TRAF6 / 樹状細胞 / FLN29 / チクングニアウイルス / ジカウイルス / IFN-β

Outline of Final Research Achievements

Using dendritic cell-specific TRAF6-deficient mice, we analyzed the role of dendritic cell subsets whose differentiation and function are controlled by TRAF6 signaling during arbovirus infection. The mutant mice showed higher viremia during Chikungunya and Zika virus infection. TRAF6-deficient dendritic cells produced lower amount of IFN-β, which may be one of causes of high susceptibility to arboviruses. Reversely, mice lacking FLN29, which binds to TRAF6 and inhibits TRAF6 signals from Toll-like receptor and RIG-I like receptor, were resistant to arbovirus infection compare to wild type mice. These findings demonstrate the important role of TRAF6 signaling in dendritic cells during arbovirus infection.

Free Research Field

免疫学、ウイルス学