タフ細胞由来IL-25は,腸内ILC2の表皮反応回路を調節する

Jakob von Moltke¹, Ming Ji^1,2, Hong-Erh Liang¹

¹Department of Medicine, University of California San Francisco, San Francisco, California 94143-0795, USA.

Nature

|December 18, 2015

まとめ

小腸のタフ細胞はIL-25を分泌し,グループ2の先天性リンパ球 (ILC2) を維持する. ヘルミントの感染で,この相互作用は2型免疫に不可欠な上皮の改造と粘液の産生を促します.

科学分野:

免疫学
胃腸内科
細胞生物学

背景:

寄生虫やアレルゲンによって引き起こされるタイプ2の免疫反応は粘液の産生と滑らかな筋肉の収縮を含みます
グループ2の先天性リンパ球細胞 (ILC2s) とTヘルパー細胞 (TH2細胞) のインタールイキン-13 (IL-13) がこれらの生理学的変化を誘導する.
IL-33,TSLP,およびIL-25のような上皮細胞性サイトカインは,ILC2sを活性化することが知られているが,その正確な起源と調節は完全に理解されていない.

研究の目的:

2型免疫における小腸タフト細胞の役割を調査する.
ILC2sを活性化する上皮信号の源と調節を解明する.
細胞回路を定義する 2型免疫応答中の上皮の再構築を媒介する

主な方法:

ネズミのヘルミント感染モデル
腸内皮質細胞とILC2の遺伝子発現とサイトカイン生成の分析
細胞系統の追跡と機能的測定

主要な成果:

タフト細胞は,静止状態でILC2ホメオスタシスを維持するインタールイキン-25 (IL-25) を構成的に発現する.
ヘルミントの感染は,タフト細胞のIL-25の産生を促進し,さらにILC2sを活性化します.
活性化されたILC2はIL-13を分泌し,上皮細胞とコップルの分化を促進する.

結論:

タフト細胞,ILC2s,および上皮原生細胞は,2型免疫における腸内上皮再構成の重要な回路を形成する.
タフト細胞由来IL-25は,ILC2の維持と"泣いて横切る"応答のオーケストレーションに不可欠です.
この回路は,粘膜の障壁で宿主防御のための協調メカニズムを強調しています.

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