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Artículo

Lack of galectin-3 increases Jagged1/Notch activation in bone marrow-derived dendritic cells and promotes dysregulation of T helper cell polarization

Fermino, Marise L.; Dergan Dylon, Leonardo SebastianIcon ; Cecílio, Nerry T.; Santos, Sofia N.; Toscano, Marta AliciaIcon ; Dias Baruffi, Marcelo; Roque Barreira, Maria C.; Rabinovich, Gabriel AdriánIcon ; Bernardes, Emerson S.
Fecha de publicación: 08/2016
Editorial: Elsevier
Revista: Molecular Immunology
ISSN: 0161-5890
e-ISSN: 1872-9142
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Bioquímica y Biología Molecular; Patología

Resumen

Galectin-3, an endogenous glycan-binding protein, is abundantly expressed at sites of inflammation and immune cell activation. Although this lectin has been implicated in the control of T helper (Th) polarization, the mechanisms underlying this effect are not well understood. Here, we investigated the role of endogenous galectin-3 during the course of experimental Leishmania major infection using galectin-3-deficient (Lgals3-/-) mice in a BALB/c background and the involvement of Notch signaling pathway in this process. Lgals3-/- mice displayed an augmented, although mixed Th1/Th2 responses compared with wild-type (WT) mice. Concomitantly, lymph node and footpad lesion cells from infected Lgals3-/- mice showed enhanced levels of Notch signaling components (Notch-1, Jagged1, Jagged2 and Notch target gene Hes-1). Bone marrow-derived dendritic cells (BMDCs) from uninfected Lgals3-/- mice also displayed increased expression of the Notch ligands Delta-like-4 and Jagged1 and pro-inflammatory cytokines. In addition, activation of Notch signaling in BMDCs upon stimulation with Jagged1 was more pronounced in Lgals3-/- BMDCs compared to WT BMDCs; this condition resulted in increased production of IL-6 by Lgals3-/- BMDCs. Finally, addition of exogenous galectin-3 to Lgals3-/- BMDCs partially reverted the increased sensitivity to Jagged1 stimulation. Our results suggest that endogenous galectin-3 regulates Notch signaling activation in BMDCs and influences polarization of T helper responses, thus increasing susceptibility to L. major infection.
Palabras clave: Galectin-3 , Leishmania Major , Notch Signaling , T Helper Response
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info:eu-repo/semantics/openAccess 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/11336/24019
URL: http://www.sciencedirect.com/science/article/pii/S0161589016301079
DOI: http://dx.doi.org/ 10.1016/j.molimm.2016.06.005
Colecciones
Articulos(IBYME)
Articulos de INST.DE BIOLOGIA Y MEDICINA EXPERIMENTAL (I)
Citación
Fermino, Marise L.; Dergan Dylon, Leonardo Sebastian; Cecílio, Nerry T.; Santos, Sofia N.; Toscano, Marta Alicia; et al.; Lack of galectin-3 increases Jagged1/Notch activation in bone marrow-derived dendritic cells and promotes dysregulation of T helper cell polarization; Elsevier; Molecular Immunology; 76; 8-2016; 22-34
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