Differential role of NADPH oxidase in autoimmune diseases

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K07294
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 48030:Pharmacology-related
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Matsumoto Misaki 京都府立医科大学, 医学(系)研究科(研究院), 助教 (80533926)
• Co-Investigator(Kenkyū-buntansha): 岩田 和実 京都府立医科大学, 医学(系)研究科(研究院), 講師 (60305571)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: NADPH oxidase / スーパーオキシド / 関節炎 / 自己免疫疾患

Outline of Final Research Achievements

Nox1 deficiency significantly suppressed the onset and severity of the LPS-induced exacerbation of collagen-induced arthritis in mice. Splenocytes from both genotypes showed similar Th1/Th17 responses at 2 weeks after the collagen immunization. On the other hand, intraperitoneal injection of LPS increased NOX1 mRNA in CD11b+ monocytes/macrophages as well as CD11c+ dendritic cells of the spleen. These results suggest that NOX1 is involved in the effector (inflammation) phase of the experimental arthritis, but not in the priming phase.

Free Research Field

薬理学

Academic Significance and Societal Importance of the Research Achievements

NOX2/NADPH oxidaseの遺伝的機能欠損は自己免疫疾患の発症リスクを増大させる。このため自己免疫疾患におけるNOX2の抑制的役割は注目されているが、発現量で劣るNOX1についてはあまり解析が進んでいなかった。本研究は、NOX1はNOX2と異なり自己免疫疾患の発症に寄与することを初めて報告したものであり、免疫系細胞におけるNOX1の新しい役割を提起するものである。