Editorial
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Cardiol. Oct 26, 2018; 10(10): 123-126
Published online Oct 26, 2018. doi: 10.4330/wjc.v10.i10.123
T-cells in myocardial infarction: Culprit instigators or mere effectors?
Luca Liberale, Aldo Bonaventura, Fabrizio Montecucco
Luca Liberale, Center for Molecular Cardiology, University of Zürich, Schlieren 8952, Switzerland
Luca Liberale, Aldo Bonaventura, Fabrizio Montecucco, First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa 16132, Italy
Fabrizio Montecucco, IRCCS Ospedale Policlinico San Martino Genoa - Italian Cardiovascular, Network, 16132 Genoa, Italy
Author contributions: Liberale L wrote the manuscript; Bonaventura A and Montecucco F revised the draft and gave suggestions for its improvement.
Conflict-of-interest statement: Liberale L, Bonaventura A and Montecucco F declare no conflict of interest related to this publication.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Luca Liberale, MD, Postdoctoral Fellow, Doctor, First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, 6 viale Benedetto XV, Genoa 16132, Italy. luca.liberale@uzh.ch
Telephone: +39-10-3537940 Fax: +39-10-3538686
Received: May 29, 2018
Peer-review started: May 29, 2018
First decision: June 14, 2018
Revised: June 20, 2018
Accepted: June 28, 2018
Article in press: June 28, 2018
Published online: October 26, 2018
Abstract

Immune system activation and dysfunction characterize the early phase of reperfusion after a myocardial infarction (MI). Despite initially neglected, adaptive immunity has been recently showed to play an important role in this setting. In fact, the immune system can recognize sequestered antigens released by the necrotic tissue, initiating a deleterious autoimmune vicious circle leading to worse outcome. In their recent work, Angelini et al shed the light on a new feature of post-MI which involves two “old players” of post-ischemic myocardial injury: CD31 and matrix metalloproteinase (MMP)-9. Specifically, the authors showed that an enhancement of MMP-9 release could determine the cleavage of inhibitory CD31 from CD4+ T-cells surface in patients with Acute Coronary Syndromes (ACS). These findings open the room for new studies investigating the role of MMP9 in other pathological processes associated with a reduction of CD31 functionality, such as plaque instability and rupture. Of interest, in the case of a causative role for CD31 shedding in ACS would be confirmed, there might be a potential role for the administration of CD31 protein or analogue compounds to blunt post-ischemic cardiac inflammation and improve ACS outcome.

Keywords: Matrix metalloproteinase, Lymphocytes, Autoimmunity, Inflammation, Myocardial infarction, Adaptive immunity

Core tip: CD31 and matrix metalloproteinases (MMP)-9 are known mediators that are upregulated during reperfusion after cardiac ischemia. By inhibiting T-cell receptor-dependent lymphocyte activation, the functional CD31 could reduce post-ischemic inflammatory response; while MMP-9 is deeply involved in inflammatory cell recruitment and myocardial remodeling. A recent paper published in European Heart Journal linked these mediators by showing CD31 cleavage to be MMP-9 dependent in patients with acute coronary syndromes (ACS). Whether this process is causative of ACS or rather its effect still needs to be clarified.