A novel regulatory mechanism for innate immune signals by ectoenzymes BST-1 and CD38

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K08943
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 54030:Infectious disease medicine-related
• Research Institution: Kawasaki Medical School
• Principal Investigator: Iseki Masanori 川崎医科大学, 医学部, 講師 (30532353)
• Co-Investigator(Kenkyū-buntansha): 石原 克彦 川崎医科大学, 医学部, 教授 (10263245) ; 矢作 綾野 川崎医科大学, 医学部, 助教 (10584873)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 辺縁帯B細胞 / マクロファージ / IL-6 / 抗体産生 / 自然免疫 / 細胞膜外酵素

Outline of Final Research Achievements

We have been clarifying that an ectoenzyme BST-1 is expressed on various immune cells. To uncover its function in vivo, we generated BST-1 gene deficient mice and analyzed their responses against antigen immunization or challenge of microbial component, LPS. Experiments were done in specific pathogen-free condition with strict experimental conditions for keeping out environmental and other effects. As a result, there was no significant differences in antibody production against thymus-independent antigens and endotoxin shock induced by LPS injection. These results indicate that BST-1 is not required for these innate-like immune responses.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

我々は予備実験においてBST-1遺伝子欠損マウスはB細胞を直接活性化できる外来抗原に対する反応が亢進しているという結果を得ていた。しかしながら動物の飼育条件や比較対照動物の選定を厳密にしてもう一度実験を行ったところ、通常のマウスと変異マウスの間で有意な反応の差は見られなかった。免疫反応は個体が生育、居住する環境から多くの影響を受ける。動物を用いて免疫反応を調べる際はそれらの条件を厳密に揃えることが正しい結果を得るために重要である。