The present study demonstrates that galectin-9 may play a crucial role in CVB3-induced myocarditis and that it may represent a novel therapeutic candidate that is able to suppress autoimmune inflammation by regulating T cell differentiation and the balance of pathogenic and regulatory T cells, such that production of pro-inflammatory cytokines are inhibited and anti-inflammatory cytokines are enhanced. Here, LGALS9 is linked to myocarditis.