アストロサイト由来のインタールイキン-33は,マイクログリアルシナプスの吸収と神経回路の発達を促進する
Ilia D Vainchtein1, Gregory Chin1, Frances S Cho2,3
1Department of Psychiatry/Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Science (New York, N.Y.)
|February 9, 2018
まとめ
中枢神経系 (CNS) のシナプス発育に不可欠である. IL-33はマイクログリアに信号を送り,シナプスの除去を促進し,神経回路の恒常性を維持します.
科学分野:
- 神経科学
- 免疫学
- 発達生物学
背景:
- シナプスの形成と再構成は,中枢神経系 (CNS) の発達と機能に不可欠である.
- 機能不全のシナプスは様々な神経発達障害に 関わっている.
- CNSのシナプス調節における先天的な免疫信号の役割は,まだほとんど研究されていない.
研究 の 目的:
- 中枢神経のシナプス発育とホメオスタシスにおけるインタールイキン-33 (IL-33) の役割を調査する.
- 中枢神経系の発達中のIL-33の細胞源と標的を明らかにする.
- マイクログリア機能とシナプス除去に対するIL-33信号伝達の影響を理解する.
主な方法:
- 中枢神経の発達中のIL-33の生成と機能を研究するためにマウスモデルを使用した.
- アストロサイトとマイクログリアのIL-33信号伝達経路を調査した.
- 脊髄とタラムスのシナプス数と神経回路の機能を評価した.
- シナプスのマイクログリアの吸収を in vivo で調べた.
主要な成果:
- 発達するアストロサイトは,サイトカインIL-33を産生する.
- IL-33は正常なシナプス数と神経回路機能を維持するために発達的に不可欠です.
- IL-33は主に生理学的条件下でマイクログリアに信号を送る.
- IL - 33はマイクログリアルシナプスの吸収を強化し,シナプスの枯渇を誘導する.
結論:
- IL-33は,中枢神経の発達中のシナプスホメオスタシスを調節する重要なサイトカインです.
- アストロサイトとマイクログリアを含むサイトカイン媒介の経路がシナプス除去を制御する.
- このメカニズムは 発達中の中枢神経系の 適切な神経回路の形成と機能に不可欠です
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