タフ細胞,味覚化学センサー細胞,腸内の寄生虫2型免疫をオーケストラ化

Michael R Howitt¹, Sydney Lavoie¹, Monia Michaud¹

¹Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA.

Science (New York, N.Y.)

|February 6, 2016

まとめ

腸のタフ細胞は寄生虫の感染時に広がってセンチネルとして機能します腸内寄生虫に対する2型免疫を促進します

科学分野:

免疫学
胃腸内科
細胞生物学

背景:

腸内皮質は腸内微生物群に対する重要な障壁です
原生体やヒルミントのような真核性腸内微生物に反応する上皮細胞の役割は完全に理解されていません.

研究の目的:

寄生虫感染に対する宿主反応における腸のタフット細胞の役割を調査する.
腸の寄生虫に対する免疫を組織するメカニズムを解明する.

主な方法:

寄生虫の植民期におけるタフト細胞集団の観察研究.
化学感知信号の遺伝的障害 (TRMP5 ノックアウト)
サイトカイン分析 (インタールイキン-25およびインタールイキン-13) と細胞集団評価 (タフト細胞,コップ細胞,エオシノフィル,タイプ2の先天性リンパ球細胞).

主要な成果:

寄生虫のコロニー化や感染でツフ細胞が蓄積されます
TRMP5媒介の化学感知信号の喪失は,タフト細胞,コップ細胞,エオシノフィル,および2型先天性リンパ性細胞の拡張を阻害する.
タフト細胞は,寄生虫によって誘発されたインタールイキン25の主な源として特定されています.
インタールイキン - 25は,先天性リンパ性細胞からのインタールイキン - 13の生成を刺激することによって,間接的にタフト細胞の膨張を促進します.

結論:

腸のタフ細胞は腸内皮質の重要な看守です
タフト細胞は,インタールイキン-25/インタールイキン-13軸を通して,腸内寄生虫に対するタイプ2の免疫反応を開始し,増幅します.

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