The role of PSGL-1-expressing CD4 T cells in the culprit lesion of acute coronary syndrome

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591073
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Circulatory organs internal medicine
• Research Institution: Tokyo Women's Medical University
• Principal Investigator: SATO Kayoko 東京女子医科大学, 医学部, 講師 (20246482)
• Co-Investigator(Kenkyū-buntansha): SUZUKI Atsushi 東京女子医科大学, 医学部, 助教 (00625626) ; SAWABE Motoji 東京医科歯科大学, その他の研究科, 教授 (30196331)
• Co-Investigator(Renkei-kenkyūsha): HAGIWARA Nobuhisa 東京女子医科大学, 医学部, 教授 (00180802)
• Research Collaborator: KITAMURA Kazutaka ; SAITO Takashi ; ENDO Keiko ; FUTASE Atsuko ; MASUDA Chieko
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: PSGL-1 / 動脈硬化 / 急性冠症候群 / 炎症 / 免疫 / 接着分子 / T細胞 / 白血球

Outline of Final Research Achievements

Adhesion of circulating leukocytes to the endothelial cells (ECs) and subsequent trans-endothelial migration are important in the development of atherosclerosis. This process is predominantly mediated by adhesion molecules, which are expressed on ECs and leukocytes. The culprit coronary artery and atherosclerotic plaque from patients with acute coronary syndrome (ACS) underwent the thrombus-aspiration therapy contained abundant PSGL-1+CD4+T cells. These PSGL-1+CD4+T cells strongly bound to both P-selectin and E-selectin, and induced EC apoptosis.
Furthermore, in apolipoprotein E (ApoE) deficient mice, the advanced atherosclerosis with many activated IFNγ+CD4 T cells, IL17+CD4 T cells, and apoptosis were observed. In contrast, these features were inhibited in PSGL-1/ApoE double deficient mice, contributing more stabilized morphologic features. We concluded that PSGL-1 expressing CD4+T cells participate directly in the development of atherosclerosis and plaque instability in ACS.

Free Research Field

医歯薬学・循環器内科学