RT Journal Article
T1 Enhanced susceptibility of galectin-1 deficient mice to experimental colitis
A1 Fernández Pérez, Raquel
A1 López Santalla, Mercedes
A1 Sánchez Domínguez, Rebeca
A1 Alberquilla, Omaira
A1 Gutiérrez Cañas, Irene
A1 Juarranz Moratilla, Yasmina
A1 Bueren, Juan A.
A1 Garin, Marina I.
AB 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.
PB Frontiers Media
YR 2021
FD 2021-06-28
LK https://hdl.handle.net/20.500.14352/106065
UL https://hdl.handle.net/20.500.14352/106065
LA eng
NO Fernandez-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.
NO Este trabajo fue subvencionado por el Instituto de Salud Carlos III y cofinanciado por el Fondo Europeo de Desarrollo Regional (FEDER)
NO Ministerio de Ciencia, Innovación y Universidades (España)
NO European Commission
DS Docta Complutense
RD 3 ago 2025