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Artículo

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

Papa Gobbi, RodrigoIcon ; Muglia, Cecilia IsabelIcon ; Rocca, Andrés; Curciarello, RenataIcon ; Sambuelli, Alicia; Martínez Yantorno, Sofía Nélida; Correa, Gustavo Javier; Morosi, Luciano GastónIcon ; Di Sabatino, Antonio; Biancheri, Paolo; MacDonald, Thomas T.; Toscano, Marta AliciaIcon ; Mariño, Karina ValeriaIcon ; Rabinovich, Gabriel AdriánIcon ; Docena, Guillermo H.Icon
Fecha de publicación: 06/2021
Editorial: Springer
Revista: Apoptosis
ISSN: 1360-8185
e-ISSN: 1573-675X
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Inmunología

Resumen

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 < 0.05) as revealed by flow cytometry using peanut agglutinin (PNA) binding and assessing dysregulation of the core-2 β 1-6-N-acetylglucosaminyltransferase 1 (C2GNT1), an enzyme responsible for elongation of core 2 O-glycans. Consequently, Gal-1 binding was attenuated in CD3+CD4+ and CD3+CD8+ LP T-cells isolated from inflamed sites (p < 0.05). Incubation with recombinant Gal-1 induced apoptosis of LP CD3+ T-cells isolated from control subjects and non-inflamed areas of IBD patients (p < 0.05), but not from inflamed areas. In conclusion, our findings showed that transient regulation of the O-glycan profile during inflammation modulates Gal-1 binding and LP T-cell survival in IBD patients.
Palabras clave: CROHN DISEASE , GALECTIN-1 , GUT , INFLAMMATION , INFLAMMATORY BOWEL DISEASE , O-GLYCOSYLATION , T-CELLS , ULCERATIVE COLITIS
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Atribución-NoComercial-SinDerivadas 2.5 Argentina (CC BY-NC-ND 2.5 AR)
Identificadores
URI: http://hdl.handle.net/11336/158881
DOI: http://dx.doi.org/10.1007/s10495-021-01675-z
URL: https://link.springer.com/article/10.1007/s10495-021-01675-z
Colecciones
Articulos(CCT - SALTA-JUJUY)
Articulos de CTRO.CIENTIFICO TECNOL.CONICET - SALTA-JUJUY
Citación
Papa Gobbi, Rodrigo; Muglia, Cecilia Isabel; Rocca, Andrés; Curciarello, Renata; Sambuelli, Alicia; et al.; Spatiotemporal regulation of galectin-1-induced T-cell death in lamina propria from Crohn’s disease and ulcerative colitis patients; Springer; Apoptosis; 26; 5-6; 6-2021; 323-337
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