Immunology
Abstract
Research Article
Authors
Lior Carmon, Irene Bobilev-Priel, Baruch Brenner, Dimitry Bobilev, Adrian Paz, Erez Bar-Haim, Boaz Tirosh, Tirza Klein, Mati Fridkin, Francois Lemonnier, Esther Tzehoval, Lea Eisenbach
Abstract
Research Article
Authors
Sophie Lanone, Tao Zheng, Zhou Zhu, Wei Liu, Chun Geun Lee, Bing Ma, Qingsheng Chen, Robert J. Homer, Jingming Wang, Lesley A. Rabach, Morgan E. Rabach, J. Michael Shipley, Steven D. Shapiro, Robert M. Senior, Jack A. Elias
Abstract
Research Article
Authors
David M. Koelle, Zhi Liu, Christopher M. McClurkan, Max S. Topp, Stanley R. Riddell, Eric G. Pamer, Andrew S. Johnson, Anna Wald, Lawrence Corey
Abstract
Research Article
Authors
Thais P. Salazar-Mather, Casey A. Lewis, Christine A. Biron
Abstract
Research Article
Authors
Kaoru Saegusa, Naozumi Ishimaru, Kumiko Yanagi, Rieko Arakaki, Kouichi Ogawa, Ichiro Saito, Nobuhiko Katunuma, Yoshio Hayashi
Abstract
Commentary
Authors
Terry Davies, Russell Marians, Rauf Latif
Abstract
Research Article
Authors
Michael J. Walter, Jeffrey D. Morton, Naohiro Kajiwara, Eugene Agapov, Michael J. Holtzman
Abstract
Research Article
Authors
Niels C. Riedemann, Ren-Feng Guo, Thomas A. Neff, Ines J. Laudes, Katie A. Keller, Vidya J. Sarma, Maciej M. Markiewski, Dimitrios Mastellos, Christoph W. Strey, Carl L. Pierson, John D. Lambris, Firas S. Zetoune, Peter A. Ward
Abstract
Research Article
Authors
Tania Nikolcheva, Stephane Pyronnet, Szu-yi Chou, Nahum Sonenberg, An Song, Carol Clayberger, Alan M. Krensky
Abstract
Group B coxsackieviral (CVB) infection commonly causes viral myocarditis. Mice are protected from CVB3 myocarditis by gene-targeted knockout of p56Lck(Lck), the Src family kinase (Src) essential for T cell activation. Extracellular signal-regulated kinase 1 and 2 (ERK-1/2) can influence cell function downstream of Lck. Using T cell lines and neonatal cardiac myocytes we investigated the role of ERK-1/2 in CVB3 infection. In Jurkat T cells ERK-1/2 is rapidly activated by CVB3; but, this response is absent in Lck-negative JCaM T cells. Inhibition of ERK-1/2 with UO126 reduced CVB3 titers in Jurkat cells, but not in JCaM cells. In cardiac myocytes CVB3 activation of ERK-1/2 is blocked by the Src inhibitor PP2. In addition, viral production in myocytes is decreased by Src or ERK-1/2 inhibition. In vitro, in both immune and myocardial cells, ERK-1/2 is activated by CVB3 downstream of Lck and other Src’s and is necessary for efficient CVB3 replication. In vivo, following CVB3 infection, ERK-1/2 activation is evident in the myocardium. ERK-1/2 activation is intense in the hearts of myocarditis-susceptible A/J mice. In contrast, significantly less ERK-1/2 activation is found in the hearts of myocarditis-resistant C57BL/6 mice. Therefore, the ERK-1/2 response to CVB3 infection may contribute to differential host susceptibility to viral myocarditis.
Authors
Mary Anne Opavsky, Tami Martino, Marlene Rabinovitch, Josef Penninger, Chris Richardson, Martin Petric, Cathy Trinidad, Lisa Butcher, Janice Chan, Peter P. Liu
Copyright © 2026 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)