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

RODRIGO PAPA-GOBBI; CECILIA I. MUGLIA; ANDRÉS ROCCA; RENATA CURCIARELLO; ALICIA M. SAMBUELLI; MARTÍN YANTORNO; GUSTAVO CORREA; LUCIANO G. MOROSI,; ANTONIO DI SABATINO; PAOLO BIANCHERI; THOMAS T. MACDONALD; MARTA A. TOSCANO; KARINA V. MARIÑO (*); GABRIEL A. RABINOVICH (*); GUILLERMO DOCENA (*)

APOPTOSIS

SPRINGER

Lugar: Berlin; Año: 2021

1360-8185

Inflammatory bowel disease (IBD), including Crohn?s disease (CD) and ulcerative colitis (UC), is characterized by chronic, relapsing intestinal inflammation. Galectin-1 (Gal-1) is an endogenous lectin with key pro-resolving roles, including induction of T-cell apoptosis and secretion of immunosuppressive cytokines. Despite considerable progress, the relevance of Gal-1-induced T-cell death in inflamed tissue from human IBD patients has not been ascertained. Intestinal biopsies and surgical specimens from control patients (n=52) and patients with active or inactive IBD (n=97) were studied. Gal-1 expression was studied by RT-qPCR, immunoblotting, ELISA and immunohistochemistry. Gal-1-specific ligands and Gal-1-induced apoptosis of lamina propria (LP) T-cells were determined by TUNEL and flow cytometry. We found a transient expression of asialo core 1-O-glycans in LP T-cells from inflamed areas (p