リンパ球における酸化した低密度リポタンパク質受容体は,動脈硬化症を予防し,臨床前疾患を予測する

Katerina Tsilingiri¹, Hortensia de la Fuente^2,3, Marta Relaño¹

¹Vascular Pathophysiology Area (K.T., M.R., R.S.-D., V.F., P.M., F.S.-M.), Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.

Circulation

|December 28, 2018

まとめ

T細胞免疫に不可欠なCD69受容体は,Th17細胞の発達を阻害することによって,動脈硬化から保護します. 患者におけるCD69値の低下は,動脈硬化のリスクの増加と相関する.

科学分野:

免疫学
心血管研究
分子生物学

背景:

Th17とT細胞は動脈硬化に関与しているが,その分子調節因子は不明である.
T細胞免疫におけるCD69受容体の役割は,動脈硬化症の発達との関連を示唆する.

研究の目的:

CD69と動脈硬化症との関連を動物モデルとヒトのサブクリニック疾患で調査する.
CD69や酸化LDL,T細胞の分化に関わる分子メカニズムを解明する.

主な方法:

リンパ性細胞にCD69が欠けている低密度の脂質タンパク質受容体を持たないマウスを使用し,高脂肪食を与えました.
PESA試験の305人の参加者において,インビトロT細胞測定を行い,CD69およびNR4A発現を分析した.

主要な成果:

リンパ性CD69が欠けていたマウスは,より大きな動脈硬化プラークと,より高いTh17/Treg比を示した.
Tリンパ球のCD69は酸化LDLと結合し,NR4A活性化によってTh17細胞を抑制する.
亜臨床性動脈硬化症の患者は白血球のCD69とNR4A1mRNAが低かった.

結論:

リンパ性細胞のCD69欠乏は,T細胞のバランスを乱すことで動脈硬化症を悪化させる.
CD69酸化されたLDLの相互作用は,抗炎症転写因子を促進する.
CD69の発現は亜臨床性動脈硬化症の独立した予測因子である.

キーワード:

CD69抗原について Th17 細胞動脈硬化症酸化された低密度リポタンパク質調節性Tリンパ球

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