感覚神経は,慢性的なを媒介する古典的な免疫信号経路をコオプトする

Landon K Oetjen¹, Madison R Mack¹, Jing Feng²

¹Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.

Cell

|September 12, 2017

まとめ

2型サイトカインは感覚神経細胞を活性化し慢性的なを引き起こします JAK阻害剤でニューロンのJAK-STAT信号を標的にすることは,患者における頑固なの治療に有望である.

科学分野:

神経科学
免疫学
皮膚科

背景:

のような哺乳類の反射は病原菌を排出しますが炎症とを結びつけるメカニズムは不明です
慢性炎症性疾患である喘息やアトピー性皮膚炎には,が伴う.
炎症経路がかゆみを促す仕組みを理解することは効果的な治療法の開発に不可欠です

研究の目的:

感覚神経細胞の活性化における2型サイトカインの直接的な役割を調査する.
慢性的なに伴う信号経路を解明するためです
慢性的なを患う患者にこれらの経路をターゲットにすることで治療の可能性を探る

主な方法:

マウスとヒトの感覚神経細胞に対する2型サイトカインの効果を研究した.
ニューロンのインタールイキン-4受容体α (IL-4Rα) とジャヌスキナーゼ1 (JAK1) のシグナル伝達に対する慢性的なの依存性を分析した.
治療に抵抗する慢性的なの患者におけるJAK阻害剤の有効性を評価した.

主要な成果:

2型サイトカインは,マウスとヒトの両方の感覚神経細胞を直接活性化することが判明しました.
慢性的なはニューロンのIL-4RαとJAK1シグナル伝達に依存することが示された.
JAK阻害剤による治療で,慢性的なが有意に改善した.

結論:

JAK-STATのような伝統的に免疫系と関連付けられている信号経路は感覚神経機能とに直接関与しています
ニューロンのIL-4RαとJAK1信号は慢性的なの重要な媒介です.
JAK阻害剤は,神経系のメカニズムを標的とした,慢性的なに対する新しい治療戦略を表しています.

キーワード:

IL-13 について IL-4 について IL-4Rα JAK1 についてアトピー性皮膚炎かゆみかゆみ感受体かゆみタイプ2 サイトカイン

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