Abstract Reactions to pathogens are usually tuned to effect immunity and limit tissue damage.With chronic infections, where immunity is unsuccessful, tissue damage would be more severe were it not for the operation of numerous host counter inflammatory events. One such event is the inhibitory effects of some galectins binding to their receptors on effector T cells. A potential downside of counter inflammatory events is that they may constrain the effectiveness of immunity to acute infections. We present evidence for this situation in mice acutely infected with Influenza A virus (IAV). We show that virus specific CD8+T cells in both bronchoalveolar lavage (BAL) and spleen up regulate Tim-3 following IAV infection. In an ex-vivo apoptosis assay, addition of Galectin-9 (Gal-9) to the splenocytes (d10pi) caused apoptosis of both Tim-3+and DbNPtet+ CD8+T cells. Furthermore, Galectin-9 knockout (G9KO) mice mounted more robust acute phase virus-specific CD8+T cell response and cleared virus more rapidly than WT mice. G9KO mice also generated higher virus specific serum IgM, IgG and a more rapid IgA response than WT. When IAV immune mice were challenged with a heterologous IAV, G9KO mice mounted a 4 fold stronger IAV specific CD8+T cell response than WT mice. Tim-3 fusion protein infusion into infected WT mice enhanced CD8+T cell responses to IAV. Our results could indicate that manipulating galectin signals may represent a convenient approach to improve immune responses to some vaccines.