"不適切な1型免疫は,粘膜菌感染症に対する感受性を誘発する"に関するコメントへの回答
Timothy J Break1, Vasileios Oikonomou1, Nicolas Dutzan2
1Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
まとめ
インターフェロノパシーは,IL-17/IL-22の自己抗体ではなく,自己免疫性多細胞症候群のカンジドアシスを誘発する. エアー不足のマウスと患者での研究は,この発見の強力な証拠を提供します.
科学分野:
- 免疫学
- 内分泌学
- 感染症
背景:
- 自身免疫性多細胞症候群 (APECED) は珍しい自己免疫性疾患である.
- IL-17/IL-22やI型インターフェロンなどのサイトカインがAPECED関連カンジダで果たす役割は議論されている.
- 以前の研究では,IL-17/IL-22の自己抗体が原因であると示唆されていたが,この研究は代替メカニズムを調査している.
研究 の 目的:
- IL-17/IL-22の自己抗体がAPECEDでカンジダシスを促進するという仮説に異議を唱える.
- APECEDにおける粘膜 кандидозの主な要因としてインターフェロナパシーを支持する証拠を提供すること.
- エア欠乏症がカンジダ症の病原性における役割を調査する.
主な方法:
- 粘膜カンジダシスを研究するために,空気不足のマウスモデルを使用した.
- マウスモデルでのインターフェロノパシーマーカーとIL-17 / IL-22応答を分析した.
- APECED患者の臨床データと免疫学的評価で裏付けられた結果
主要な成果:
- エアー欠乏症のマウスの 粘膜腺炎を誘発することが示されました
- 感染したマウスでは,自己抗体仮説に反する,完ぺきなIL-17/IL-22反応が観察された.
- インターフェロノパシーとカンジダースの関連性を示す 強力な証拠がAPECEDで発見されました
結論:
- インターフェロノパシーは,APECEDにおける粘膜腺炎を促す主なメカニズムである.
- この文脈におけるIL-17/IL-22自己抗体の役割は二次的または軽微である可能性が高い.
- 空気の欠乏は,インターフェロノパシーによるカンジダの病原化に寄与する.
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