As for Th17 immunity responsible for clearing bacterial infection, our results demonstrate a dispensable role for Lgals3 in clearing C. rodentium infection, which is consistent with a previous observation.44 Interestingly, although we observed upregulation of Lgals3 in CD4+ T cells during EAE development, Lgals3 was not upregulated in colonic CD4+ T cells in response to C. rodentium infection, suggesting a tissue-specific function for Lgals3 and supports the selective requirement for Lgals3 in EAE development but not in C. rodentium infection clearance. This evidence concerns the gene LGALS3 and bacterial infectious disease.