Fc受容体イソフォームは,細胞プラズマ領域の異質性の結果として,コーティングピット局所化のための明確な能力を発揮します
H M Miettinen1, J K Rose, I Mellman
1Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510.
Cell
|July 28, 1989
まとめ
マウスのマクロファージとリンパ球は,IgGに対する独特のFc受容体を持っています. マクロファージのFc受容体 (FcRII-B2) の特定の細胞質尾領域は,リンパ球同型 (FcRII-B1) と異なり,効率的な内部化に不可欠です.
科学分野:
- 免疫学 免疫学とは
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- マクロファージとリンパ球は,IgG Fc受容体の異なる同型を発現する.
- これらのアイソフォーム,FcRII-B1 (リンパ球) とFcRII-B2 (マクロファージ) は,代替 mRNA スプライシングにより異なる.
- FcRII-B1は,FcRII-B2 (47アミノ酸) よりもサイトプラズマ尾 (94アミノ酸) が長い.
研究 の 目的:
- FcRII-B1とFcRII-B2.2の間の細胞質ドメインの変動の機能的重要性を調査する.
- FcRII-B1の拡張された細胞質尾が,Fc受容体の機能にどのように影響するかを決定する.
主な方法:
- 2つのFc受容体イソフォーム (FcRII-B1およびFcRII-B2) の発現は,受容体陰性線維芽細胞に存在する.
- 各同型によって媒介されるリガンド内在化とリソソーム配分の分析.
- クラトリンで覆われた穴の内での受容体の局所化の評価.
主要な成果:
- FcRII-B2が媒介する効率的なリガンド内化とリソソーム配送.
- FcRII-B1経由のエンドサイトーシスとテイルマイナス変異体は,効率が著しく低下した.
- FcRII-B1と尾のマイナス変異体は,クラスリンで覆われた穴に蓄積できませんでした.
結論:
- FcRII-B2の細胞質尾には,クラスリンで覆われた穴の蓄積に不可欠なドメインが含まれています.
- この重要な領域は,FcRII-B1イソフォームに存在する47アミノ酸挿入によって破壊されます.
- 細胞プラズマ尾の構造は,Fc受容体の局所化と内細胞効率を左右する.
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