Search for new molecules controlling the response of nucleic acid-sensing TLRs

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460585
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: The University of Tokyo
• Principal Investigator: FUKUI Ryutaro 東京大学, 医科学研究所, 助教 (60554508)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 自然免疫 / 自己免疫疾患 / Toll-like receptor / 核酸認識 / I型インターフェロン / Unc93 homolog B1 / 新規分子探索

Outline of Final Research Achievements

We tried functional cloning to find new molecules controlling the response of nucleic acid-sensing Toll-like receptors (TLRs), like TLR7. As the other way, we analyzed the phenotype of Unc93 homolog B1 (Unc93B1) D34A mutant mice, which suffer from systemic inflammation caused by TLR7 hyperactivation
As results, we found that the phenotype of D34A mice was attenuated by lacking type I interferon receptor (IFNAR1). Type I IFN signaling maintained the expression of TLR7 in B cells, and the number of TLR7-expressing conventional dendritic cells, respectively.

Free Research Field

免疫学