Spatiotemporal regulation of galectin-1-induced T-cell death in lamina propria from Crohn's disease and ulcerative colitis patients.

摘要: Inflammatory bowel disease (IBD), including Crohn's (CD) and ulcerative colitis (UC), is characterized by chronic, relapsing intestinal inflammation. Galectin-1 (Gal-1) an endogenous lectin with key pro-resolving roles, induction of T-cell apoptosis secretion immunosuppressive cytokines. Despite considerable progress, the relevance Gal-1-induced death in inflamed tissue from human IBD patients has not been ascertained. Intestinal biopsies surgical specimens control (n = 52) active or inactive 97) were studied. Gal-1 expression was studied RT-qPCR, immunoblotting, ELISA immunohistochemistry. Gal-1-specific ligands lamina propria (LP) T-cells determined TUNEL flow cytometry. We found a transient asialo core 1-O-glycans LP areas (p < 0.05) as revealed cytometry using peanut agglutinin (PNA) binding assessing dysregulation core-2 β 1-6-N-acetylglucosaminyltransferase 1 (C2GNT1), enzyme responsible for elongation 2 O-glycans. Consequently, attenuated CD3+CD4+ CD3+CD8+ isolated sites 0.05). Incubation recombinant induced CD3+ subjects non-inflamed 0.05), but areas. In conclusion, our findings showed that regulation O-glycan profile during inflammation modulates survival patients.