Fernández Pérez, RaquelLópez Santalla, MercedesSánchez Domínguez, RebecaAlberquilla, OmairaGutiérrez Cañas, IreneJuarranz Moratilla, YasminaBueren, Juan A.Garin, Marina I.2024-07-122024-07-122021-06-28Fernandez-Perez R, Lopez-Santalla M, Sánchez-Domínguez R, Alberquilla O, Gutiérrez-Cañas I, Juarranz Y, Bueren JA and Garin MI (2021) Enhanced Susceptibility of Galectin-1 Deficient Mice to Experimental Colitis. Front. Immunol. 12:687443.10.3389/fimmu.2021.687443https://hdl.handle.net/20.500.14352/106065Este trabajo fue subvencionado por el Instituto de Salud Carlos III y cofinanciado por el Fondo Europeo de Desarrollo Regional (FEDER)Galectin-1 is a<jats:italic>β</jats:italic>-galactoside-binding lectin, ubiquitously expressed in stromal, epithelial, and different subsets of immune cells. Galectin-1 is the prototype member of the galectin family which shares specificity with<jats:italic>β</jats:italic>-galactoside containing proteins and lipids. Immunomodulatory functions have been ascribed to endogenous galectin-1 due to its induction of T cell apoptosis, inhibitory effects of neutrophils and T cell trafficking. Several studies have demonstrated that administration of recombinant galectin-1 suppressed experimental colitis by modulating adaptive immune responses altering the fate and phenotype of T cells. However, the role of endogenous galectin-1 in intestinal inflammation is poorly defined. In the present study, the well-characterized acute dextran sulfate sodium (DSS)-induced model of ulcerative colitis was used to study the function of endogenous galectin-1 during the development of intestinal inflammation. We found that galectin-1 deficient mice (<jats:italic>Lgals1<jats:sup>−/−</jats:sup></jats:italic>mice) displayed a more severe intestinal inflammation, characterized by significantly elevated clinical scores, than their wild type counterparts. The mechanisms underlying the enhanced inflammatory response in colitic<jats:italic>Lgals1<jats:sup>−/−</jats:sup></jats:italic>mice involved an altered Th17/Th1 profile of effector CD4<jats:sup>+</jats:sup>T cells. Furthermore, increased frequencies of Foxp3<jats:sup>+</jats:sup>CD4<jats:sup>+</jats:sup>regulatory T cells in colon lamina propria in<jats:italic>Lgals1<jats:sup>−/−</jats:sup></jats:italic>mice were found. Strikingly, the exacerbated intestinal inflammatory response observed in<jats:italic>Lgals1<jats:sup>−</jats:sup></jats:italic><jats:sup>/</jats:sup><jats:italic><jats:sup>−</jats:sup></jats:italic>mice was alleviated by adoptive transfer of wild type Foxp3<jats:sup>+</jats:sup>CD4<jats:sup>+</jats:sup>regulatory T cells at induction of colitis. Altogether, these data highlight the importance of endogenous galectin-1 as a novel determinant in regulating T cell reactivity during the development of intestinal inflammation.engAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/journal article1664-3224https://doi.org/10.3389/fimmu.2021.687443open access57.083615.37616.348-002Galectin-1Inflammatory bowel diseaseImmune regulationDSSCell therapyRegulatory T cellsInmunología3207.10 Inmunopatología