SIRPalphaまたはcalreticulin/CD91と結合することにより,肺コレクチンは二重機能の監視分子として作用し,炎症を抑制または強化します
Shyra J Gardai1, Yi-Qun Xiao, Matthew Dickinson
1Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.
Cell
|October 9, 2003
まとめ
肺表面活性タンパク質AとD (SP-AとSP-D) は,炎症において二重の役割を果たしています. 彼らの結合方向は,炎症反応を抑制するか強化するか,肺ホメオスタシスを維持するかどうかを決定します.
科学分野:
- 肺免疫学について
- 分子生物学は分子生物学である.
- ホスト-病原体相互作用
背景:
- 表面活性物質タンパク質AとD (SP-AとSP-D) は,生まれながらの免疫に不可欠な肺コレクチンである.
- これらのタンパク質は,異なるドメインを有する:PAMP結合のための球状の頭と,ファゴサイトーシスの開始のためのコラーゲン状の尾.
- 肺炎の調節におけるそれらの正確な役割については,さらなる解明が必要である.
研究 の 目的:
- 炎症媒介体の生成を調節するSP-AとSP-Dの二重の役割を調査する.
- SP-AおよびSP-D結合方向が炎症信号伝達経路に影響を与えるメカニズムを解明する.
主な方法:
- SIRPalphaとcalreticulin/CD91との調査されたSP-AとSP-Dの相互作用
- これらの相互作用が,炎症促進媒介体の生成に与える影響を分析した.
- 異なる結合指向の機能的結果を探求するためにモデルシステムを利用しました.
主要な成果:
- 球状頭経由でSIRPalphaに結合するSP-AとSP-Dは,炎症促進媒介体の生成を抑制する.
- SP-AとSP-Dがコラーゲン状の尾を介してカルレチクーリン/CD91に結合すると,炎症促進媒介体の生成を刺激する.
- SP-AとSP-Dの結合方向は,肺炎に対するそれらの純効果を決定する.
結論:
- SP-AとSP-Dは,肺炎における複雑で文脈に依存する役割を果たします.
- これらのタンパク質は,SIRPalpha経由で炎症を抑制することによって,肺ホメオスタシスの維持に貢献します.
- 特定の条件下で,SP-AとSP-Dは,病原体のクリアランスと組織修復に不可欠な炎症反応を促進することができます.
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