University of the Ryukyus · Tropical Biosphere Research Center · 准教授

Research keywordsImmunology of Host Defence Against Infectious Diseases・感染症学・生物学・基礎生命科学

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• IL-35 May Prevent the Exacerbation of Aspiration Pneumonia Involving Porphyromonas gingivalis by Suppressing IL-17 Production2025 · Kawamura, S; Goto, H; Kikuchi, T; Okabe, T; Hasegawa, Y; Sugita, Y; Fujitsuka, H; Kataoka, R; Katsumata, K; Goto, R; Suzuki, Y; Hayashi, JI; Umemura, M; Mitani, A
• 抗酸菌感染におけるCard9の機能解析(Analysis of Card9 function in pulmonary mycobacterial infection)2022 · 豊永 憲司, 梅村 正幸, 松崎 吾朗, 原 博満, 田中 芳彦, 山崎 晶
• TREM2 is a receptor for non-glycosylated mycolic acids of mycobacteria that limits anti-mycobacterial macrophage activation2021 · Mycobacterial cell-wall glycolipids elicit an anti-mycobacterial immune response via FcRγ-associated C-type lectin receptors, including Mincle, and caspase-recruitment domain family member 9 (CARD9). Additionally, mycobacteria harbor immuno-evasive cell-wall lipids associated with virulence and latency; however, a mechanism of action is unclear. Here, we show that the DAP12-associated triggering receptor expressed on myeloid cells 2 (TREM2) recognizes mycobacterial cell-wall mycolic acid (MA)-containing lipids and suggest a mechanism by which mycobacteria control host immunity via TREM2. Macrophages respond to glycosylated MA-containing lipids in a Mincle/FcRγ/CARD9-dependent manner to produce inflammatory cytokines and recruit inducible nitric oxide synthase (iNOS)-positive mycobactericidal macrophages. Conversely, macrophages respond to non-glycosylated MAs in a TREM2/DAP12-dependent but CARD9-independent manner to recruit iNOS-negative mycobacterium-permissive macrophages. Furthermore, TREM2 deletion enhances Mincle-induced macrophage activation in vitro and inflammation in vivo and accelerates the elimination of mycobacterial infection, suggesting that TREM2-DAP12 signaling counteracts Mincle-FcRγ-CARD9-mediated anti-mycobacterial immunity. Mycobacteria, therefore, harness TREM2 for immune evasion.
• Porphyromonas gingivalis components/secretions synergistically enhance pneumonia caused by Streptococcus pneumoniae in mice2021 · Okabe, T., Kamiya, Y., Kikuchi, T., Goto, H., Umemura, M., Suzuki, Y., Sugita, Y., Naiki, Y., Hasegawa, Y., Hayashi, J., Kawamura, S., Sawada, N., Takayanagi, Y., Fujimura, T., Higuchi, N., Mitani, A.

• 結核菌の病原因子Zmp1による炎症性サイトカイン遺伝子の発現制御機構の解明2025 · 基盤研究(C)
• 結核菌感染肺における3型免疫応答メカニズムの解明および抗結核ワクチン戦略の構築2025 · 基盤研究(C)
• キーストーン細菌である歯周病菌は肺炎クラミジア感染や動脈硬化を増悪化するか？2023 · 基盤研究(C)
• 免疫受容体シグナル関連分子を介した口腔カンジダ症病態制御機構の解明2023 · 基盤研究(B)

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