Skip to main content
main-content

01.01.2012 | Original Contribution | Ausgabe 1/2012

Basic Research in Cardiology 1/2012

Regulatory T cells ameliorate cardiac remodeling after myocardial infarction

Zeitschrift:
Basic Research in Cardiology > Ausgabe 1/2012
Autoren:
Ting-Ting Tang, Jing Yuan, Zheng-Feng Zhu, Wen-Cai Zhang, Hong Xiao, Ni Xia, Xin-Xin Yan, Shao-Fang Nie, Juan Liu, Su-Feng Zhou, Jing-Jing Li, Rui Yao, Meng-Yang Liao, Xin Tu, Yu-Hua Liao, Xiang Cheng
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1007/​s00395-011-0232-6) contains supplementary material, which is available to authorized users.
T.-T. Tang and J. Yuan contributed equally to this study.

Abstract

Persistent inflammatory responses participate in the pathogenesis of adverse ventricular remodeling after myocardial infarction (MI). We hypothesized that regulatory T (Treg) cells modulate inflammatory responses, attenuate ventricular remodeling and subsequently improve cardiac function after MI. Acute MI was induced by ligation of the left anterior descending coronary artery in rats. Infiltration of Foxp3+ Treg cells was detected in the infarcted heart. Expansion of Treg cells in vivo by means of adoptive transfer as well as a CD28 superagonistic antibody (JJ316) resulted in an increased number of Foxp3+ Treg cells in the infarcted heart. Subsequently, rats with MI showed improved cardiac function following Treg cells transfer or JJ316 injection. Interstitial fibrosis, myocardial matrix metalloproteinase-2 activity and cardiac apoptosis were attenuated in the rats that received Treg cells transfer. Infiltration of neutrophils, macrophages and lymphocytes as well as expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β were also significantly decreased, and the CD8+ cardiac-specific cytotoxic T lymphocyte response was inhibited. Expression of interleukin (IL)-10 in the heart, however, was increased. Additional studies in vitro indicated that Treg cells directly protect neonatal rat cardiomyocytes against LPS-induced apoptosis, and this protection depends on the cell–cell contact and IL-10 expression. Furthermore, Treg cells inhibited proinflammatory cytokines production by cardiomyocytes. These data demonstrate that Treg cells serve to protect against adverse ventricular remodeling and contribute to improve cardiac function after myocardial infarction via inhibition of inflammation and direct protection of cardiomyocytes.

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

★ PREMIUM-INHALT
e.Med Interdisziplinär

Mit e.Med Interdisziplinär erhalten Sie Zugang zu allen CME-Fortbildungen und Fachzeitschriften auf SpringerMedizin.de. Zusätzlich können Sie eine Zeitschrift Ihrer Wahl in gedruckter Form beziehen – ohne Aufpreis.

Jetzt e.Med zum Sonderpreis bestellen!

Weitere Produktempfehlungen anzeigen
Zusatzmaterial
Supplementary material 1 (PDF 113 kb)
395_2011_232_MOESM1_ESM.pdf
Literatur
Über diesen Artikel

Weitere Artikel der Ausgabe 1/2012

Basic Research in Cardiology 1/2012 Zur Ausgabe
  1. Sie können e.Med Innere Medizin 14 Tage kostenlos testen (keine Print-Zeitschrift enthalten). Der Test läuft automatisch und formlos aus. Es kann nur einmal getestet werden.


 

Neu im Fachgebiet Kardiologie

Mail Icon II Newsletter

Bestellen Sie unseren kostenlosen Newsletter Update Kardiologie und bleiben Sie gut informiert – ganz bequem per eMail.

Bildnachweise