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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.

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