アポトーシスは,ファゴサイトからのCD31媒介の細胞分離を無効化し,結合と吸収を促進します
Simon Brown1, Isabelle Heinisch, Ewan Ross
1Inflammation Repair Group, MRC Centre for Inflammation Research, University of Edinburgh, Edinburgh EH8 9AG, UK. simon.brown@ed.ac.uk
Nature
|July 12, 2002
まとめ
血小板内皮細胞粘着分子-1 (CD31) は,マクロファージから活性の高い細胞を積極的に排斥する. アポトーシスでは,CD31結合機能が変化し,マクロファージによる死滅する細胞の吸収を促進します.
科学分野:
- 免疫学 免疫学とは
- 細胞生物学 細胞生物学
- バイオケミストリー バイオケミストリー
背景:
- マクロファージはアポプトシス細胞を包み込み,組織損傷を防止し,免疫反応を調節する.
- マクロファージによって生存可能な細胞とアポプトティック細胞を区別するメカニズムは完全に理解されていません.
- 活性の高い細胞のファゴシトーシスを防止する細胞表面分子の役割は不明である.
研究 の 目的:
- 生存可能な白血球とアポプトティック白血球の間のマクロファージの差別化の分子機構を調査する.
- 活性の高い細胞の活発な排斥とアポプトティック細胞の結合を媒介する細胞表面分子を特定する.
- マクロファージと白血球の相互作用を調節するCD31の役割を明らかにする.
主な方法:
- 流れの条件下で,活性の高い白血球とアポプトティック白血球のマクロファージ結合を研究した.
- 白血球におけるCD31のホモフィル結合を調査した.
- 分析された温度依存の脱離と,低切断ストレス下での結合.
主要な成果:
- 活性の高い白血球に対するホモフィルのCD31結合は,低剪定下でのアクティブで温度に依存する脱離を促進しました.
- CD31媒介による脱離は,アポプトス性白血球において低下した.
- アポプトシス細胞の脱離の障害は,緊密に結合し,その後マクロファージの摂取につながった.
結論:
- CD31は細胞表面の分子として作用し,脱離信号を伝達することによって,生存可能な細胞のファゴサイトの摂取を防ぐ.
- CD31の機能はアポトーシスによってシフトし,死にゆく細胞がファゴサイトに結合することを促進します.
- このメカニズムは,マクロファージが生存可能な細胞とアポプトティックな細胞を区別し,相互作用する方法を説明します.
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