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Dectin-1は,マクロファージの極化と中性粒子の浸透を調節することによって,心筋不全/再注射損傷に寄与する
Qin Fan1,2, Rong Tao1, Hang Zhang1,2
1Departments of Cardiology (Q.F., R.T., H.Z., H.X., L.L., J.H., Q.Z., W.S., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China.
Circulation
|December 28, 2018
まとめ
Dectin-1は,炎症と免疫細胞の浸透を促進することによって,心筋不全/再注射 (IR) 損傷において重要な役割を果たします. Dectin- 1を阻害すると,心臓機能が改善され,心臓発作の回復のための潜在的な治療目標となる.
科学分野:
- 免疫学
- 心臓病科
- 分子生物学
背景:
- マクロファージに関連した免疫反応は,心筋不全/再注射 (IR) 損傷において重要な役割を果たします.
- 骨髄細胞のパターン認識受容体であるデクチン-1は免疫ホメオスタシスを調節するが,心筋のIR損傷におけるその役割は不明である.
研究 の 目的:
- 心筋のIR損傷におけるDectin-1の機能的意義を調査する.
- ミオカルディア IR 損傷の潜在的治療標的としてDectin-1を調査する.
主な方法:
- ネズミの遺伝子剥離,抗体阻害,デクチン-1活性化モデルを使用した.
- 免疫細胞の浸透と炎症をフローサイトメトリー,qPCR,免疫ヒストケミストリーで分析した.
- STセグメント上昇性心筋梗塞の患者におけるDectin-1+細胞レベルを評価した.
主要な成果:
- 心臓のIR損傷後のマクロファージのデクチン-1発現が増加した.
- デクチン-1欠乏症は心臓機能を改善し,アポトーシスを減少させ,M1マクロファージの偏分化と免疫細胞の浸透を減少させた.
- Dectin- 1はCxcl1とG- CSF経由で中性粒子の増殖を促進し,IL- 23/ IL- 1βの生成は,γδT細胞によるIL- 17A発現に不可欠であった.
- 循環中のDectin- 1+単細胞濃度の上昇は,心筋梗塞患者で観察され,心機能不全と相関していました.
結論:
- Dectin-1は,心筋のIR損傷を媒介する上で重要な役割を果たします.
- ミオカルディア IR 損傷に対する有望な治療戦略です.
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