サトウ カヨコ   SATO Kayoko
  佐藤 加代子
   所属   医学部 医学科(東京女子医科大学病院)
   職種   准教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 P-Selectin Glycoprotein Ligand-1 (PSGL-1) Expressing CD4 T Cells Contribute Plaque Instability in Acute Coronary Syndrome.
掲載誌名 正式名:Circulation journal : official journal of the Japanese Circulation Society
略  称:Circ J
ISSNコード:1346-9843/1347-4820
掲載区分国内
出版社 Japanese Circulation Society
巻・号・頁 82(8),2128-2135頁
著者・共著者 KITAMURA Kazutaka†, SATO Kayoko*, SAWABE Motoji, YOSHIDA Masayuki, HAGIWARA Nobuhisa
発行年月 2018/07
概要 Background: Adhesion molecules have essential roles in the development of atherosclerosis. We investigated whether P-selectin glycoprotein ligand-1 (PSGL-1)-expressing CD4 T cells contribute to plaque instability in acute coronary syndrome (ACS).

Methods and Results: We studied the adhesion molecules on CD4 T cells from consecutive patients with ACS treated with thrombus-aspirating device and compared them with healthy controls (n=48 each). Blood, thrombi, and plaque samples from the culprit coronary arteries were collected by thrombus aspiration performed during emergency coronary artery angiography. According to flow cytometry results, peripheral CD4 T cells from ACS patients strongly expressed PSGL-1 and integrin β2 (P<0.05 for both) more than those from controls; culprit coronary arteries contained an abundance of PSGL-1+ (P<0.001) but not integrin β2+CD4 T cells. In addition, immunohistochemical analysis of the thrombus-aspirating device samples revealed numerous PSGL-1+CD4 T cells in plaques from the culprit lesions. Results from the selectin-binding assay demonstrated that activated PSGL-1+CD4 T cells from ACS patients bound to P- or E-selectin after triggering the T-cell receptor, and adhered to endothelial cells under laminar flow conditions (P<0.05 and P<0.05, respectively), inducing their apoptosis (P<0.01) via activated caspase-3, which correlated with PSGL-1 expression (R=0.788, P=0.021) and was suppressed by application of a PSGL-1-specific antibody (P<0.05).

Conclusions: PSGL-1 contributed to cytotoxic CD4 T cell homing to the culprit coronary artery and promoted plaque instability in ACS.
DOI 10.1253/circj.CJ-17-1270
PMID 29962384