Galectin-8 (Gal-8) is a mammalian β-galactoside-binding lectin， endowed with proinflammatory properties. Given its capacity to enhance antigen-specific immune responses in vivo， we investigated whether Gal-8 was also able to promote APC activation to sustain T cell activation after priming. Both endogenous [dendritic cells (DCs)] and bone marrow-derived DCs (BMDCs) treated with exogenous Gal-8 exhibited a mature phenotype characterized by increased MHC class II (MHCII)， CD80， and CD86 surface expression. Moreover， Gal-8-treated BMDCs (Gal-8-BMDCs) stimulated antigen-specific T cells more efficiently than immature BMDCs (iBMDCs). Proinflammatory cytokines IL-3， IL-2， IL-6， TNF， MCP-1， and MCP-5， as well as growth factor G-CSF， were augmented in Gal-8-BMDC conditioned media， with IL-6 as the most prominent. Remarkably， BMDCs from Gal-8-deficient mice ( BMDC) displayed reduced CD86 and IL-6 expression and an impaired ability to promote antigen-specific CD4 T cell activation. To test if Gal-8-induced activation correlates with the elicitation of an effective immune response， soluble Gal-8 was coadministrated with antigen during immunization of BALB/cJ mice in the experimental foot-and-mouth disease virus (FMDV) model. When a single dose of Gal-8 was added to the antigen formulation， an increased specific and neutralizing humoral response was developed， sufficient to enhance animal protection upon viral challenge. IL-6 and IFN-γ， as well as lymphoproliferative responses， were also incremented in Gal-8/antigen-immunized animals only at 48 h after immunization， suggesting that Gal-8 induces the elicitation of an inflammatory response at an early stage. Taking together， these findings argue in favor of the use of Gal-8 as an immune-stimulator molecule to enhance the adaptive immune response.