2018 Fiscal Year Final Research Report

The requirement of B cell-intrinsic TLR7 for the protection of retrovirus-induced leuchemia

Research Project

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Project/Area Number	16K08749
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Experimental pathology
Research Institution	Baika Women's University (2017-2018) Kindai University (2016)
Principal Investigator	Sachiyo Kawahara 梅花女子大学, 食文化学部, 教授 (60297629)
Co-Investigator(Kenkyū-buntansha)	本園千尋九州大学, 医学研究院, 助教 (10642910) 宮澤正顯近畿大学, 医学部, 教授 (60167757)
Project Period (FY)	2016-04-01 – 2019-03-31
Keywords	B細胞 / 中和抗体 / レトロウイルス / TLR7 / ウイルス誘発がん
Outline of Final Research Achievements	TLR7 is expressed on several types of cell including dendritic cells and B cells. In this study, we analyzed the requirement of B-cell intrinsic TLR7 for the protection of retrovirus-induced leukemia. Mice lacking of B cell-intrinsic TLR7 produced virus-neutralizing antibodies as efficiently as the wild-type mice by priming of T helper cells, and rapid elimination of exogenous retroviruses were observed. Nevertheless,the B cell-intrinsic TLR7 lacking mice later died of leukemia. These results suggest that B cell-intrinsic TLR7 is essential to regulate the appearance of endogenous and/or recombinant retroviruses even when the virus-specific Th cells are efficiently activated.
Free Research Field	生体防御
Academic Significance and Societal Importance of the Research Achievements	本研究は、B細胞に発現する自然免疫センサーであるウイルス核酸受容体TLR7が、レトロウイルス感染誘発白血病の発症を制御すること、またその白血病発症に内在性レトロウイルスが関与している可能性を示唆した。自然免疫センサーは自己成分の内因性物質にも応答するポテンシャルがあることからも、本研究成果は、ウイルス感染の新たな制御・予防法の開発だけでなく自己免疫疾患等の発症機序を考える上でも有用な情報になると考える。