| First Author | Fernandez-Perez R | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 687443 | PubMed ID | 34262567 |
| Mgi Jnum | J:312798 | Mgi Id | MGI:6729333 |
| Doi | 10.3389/fimmu.2021.687443 | Citation | Fernandez-Perez R, et al. (2021) Enhanced Susceptibility of Galectin-1 Deficient Mice to Experimental Colitis. Front Immunol 12:687443 |
| abstractText | Galectin-1 is a beta-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 beta-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 (Lgals1(-/-) 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 Lgals1(-/-) mice involved an altered Th17/Th1 profile of effector CD4(+) T cells. Furthermore, increased frequencies of Foxp3(+)CD4(+) regulatory T cells in colon lamina propria in Lgals1(-/-) mice were found. Strikingly, the exacerbated intestinal inflammatory response observed in Lgals1(-) (/) (-) mice was alleviated by adoptive transfer of wild type Foxp3(+)CD4(+) 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. |
