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Because MS\u2010induced inflammation may decrease SVZ proliferation and thus limit repair, we studied the role of galectin\u20103 (Gal\u20103), a proinflammatory protein. Gal\u20103 expression was increased in periventricular regions of human MS in post\u2010mortem brain samples and was also upregulated in periventricular regions in a murine MS model, Theiler's murine encephalomyelitis virus (TMEV) infection. Whereas TMEV increased SVZ chemokine (CCL2, CCL5, CCL, and CXCL10) expression in wild type (WT) mice, this was inhibited in <jats:italic>Gal\u20103<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice. Though numerous CD45+ immune cells entered the SVZ of WT mice after TMEV infection, their numbers were significantly diminished in <jats:italic>Gal\u20103<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice. TMEV also reduced neuroblast and proliferative SVZ cell numbers in WT mice but this was restored in <jats:italic>Gal\u20103<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice and was correlated with increased numbers of doublecortin+ neuroblasts in the corpus callosum. In summary, our data showed that loss of Gal\u20103 blocked chemokine increases after TMEV, reduced immune cell migration into the SVZ, reestablished SVZ proliferation and increased the number of progenitors in the corpus callosum. These results suggest Gal\u20103 plays a central role in modulating the SVZ neurogenic niche's response to this model of MS. 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