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Cardiovascular Research Advance Access originally published online on July 1, 2009
Cardiovascular Research 2009 84(3):425-433; doi:10.1093/cvr/cvp219
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Amelioration of myocarditis by HVEM-overexpressing dendritic cells through induction of IL-10-producing cells

Gang Cai1, Huaizhou Wang1, Qin Qin1, Jun Zhang1, Zhi Zhu2, Menglei Liu1 and Qian Shen1,*

1 Department of Experimental Diagnosis, Shanghai Changhai Hospital, 168 Changhai road, Shanghai 200433, People's Republic of China
2 Department of Pathology, Shanghai Changhai Hospital, Shanghai, People's Republic of China

* Corresponding author. Tel: +86 21 8187 3611; fax: +86 21 8187 3611. E-mail address: laoshenqch{at}yahoo.cn

Aims: Herpes virus entry mediator (HVEM) is considered to be a molecular ‘switch’ for immune responses, and a role in immune modification has been reported. The aim of this study was to assess whether HVEM-mediated immune suppression could protect against experimental autoimmune myocarditis (EAM) induced by myosin.

Methods and results: We constructed HVEM-expressing adenovirus (AdHVEM) and fusion protein HVEM-Ig and evaluated their roles in immunoregulation in vitro and in vivo. Immunoregulation of dendritic cells (DCs) infected with recombinant virus or treated with HVEM-Ig was then studied. DCs transfected with AdHVEM (DC-AdHVEM) were protected against EAM, whereas HVEM-Ig had no protective effect. Further study showed that DC-AdHVEMs produced a regulatory cytokine, IL-10, which had further effects on induction of IL-10 producing CD4+ T cells. This subset of T cells was then responsible for the protection against EAM.

Conclusion: Myosin-DC-AdHVEM cell gene therapy appears to be a safe and effective way of inhibiting the development of EAM. The signal induced by HVEM seems to play different roles in different cells.

KEYWORDS Experimental autoimmune myocarditis; Herpes virus entry mediator; Immune regulation; Dendritic cells; IL-10

Time for primary review: 35 days


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