皮質内プラズマ網膜のストレスが,保護性IgA反応を誘導する
Joep Grootjans1,2, Niklas Krupka1,3, Shuhei Hosomi1,4
1Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Science (New York, N.Y.)
|March 2, 2019
まとめ
腸内網膜 (ER) のストレスは,T細胞独立の免疫グロブリンA (IgA) 反応を誘発する. この経路は腹腔内B1b細胞を巻き込み,腸のバリア機能を強化し,炎症から保護します.
科学分野:
- 免疫学
- 胃腸内科
- 細胞生物学
背景:
- 免疫グロブリンA (IgA) は粘膜免疫に不可欠であり,腸内微生物群を調節し,病原体の侵入を防ぐ.
- IgAの生成はT細胞依存性およびT細胞依存性 (TI) 経路によって媒介され,TIの調節はあまり理解されていない.
- 腸内皮質細胞 (IEC) エンドプラズマ網膜 (ER) のストレスは,様々な腸内疾患に関与しています.
研究 の 目的:
- IEC ERのストレスがTI IgA反応の調節における役割を調査する.
- IEC ERのストレスとIgAの産生を結びつける細胞メカニズムを解明する.
- このTI IgA反応が腸内炎症に対する保護を与えるかどうかを判断する.
主な方法:
- IECにおけるERストレス誘導
- 腹膜B1b細胞の活性化と膨張の分析
- ラミナ・プロピアとルメンのIgA濃度の定量化
- 欠陥のある自食性の個体からのヒトデータとの相関関係
主要な成果:
- IEC ERのストレスは,多活性,TI IgA反応を誘発する.
- この反応は微生物群とは無関係で,腹膜B1b細胞の活性化を伴う.
- 腸内でのIgAの産生が増加し,バリアの保護が強化された.
- 欠陥のあるオートファジーとERストレスを持つヒトでは,IgAを産生するプラズマ細胞の値が上昇した.
結論:
- IEC ERのストレスは,保護的で微生物群から独立したTI IgA経路を活性化します.
- 腹腔内B1b細胞は,IEC ERストレスと強化された腸内IgAを結びつける重要な媒介です.
- このメカニズムは 腸の障壁を保護する 新しい先天的な免疫反応を表しています
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