RBP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes
Protein & Cell
; (12): 201-209, 2016.
Article
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| WPRIM
| ID: wpr-757147
Biblioteca responsable:
WPRO
ABSTRACT
Development of alternatively activated (M2) macrophage phenotypes is a complex process that is coordinately regulated by a plethora of pathways and factors. Here, we report that RBP-J, a DNA-binding protein that integrates signals from multiple pathways including the Notch pathway, is critically involved in polarization of M2 macrophages. Mice deficient in RBP-J in the myeloid compartment exhibited impaired M2 phenotypes in vivo in a chitin-induced model of M2 polarization. Consistent with the in vivo findings, M2 polarization was partially compromised in vitro in Rbpj-deficient macrophages as demonstrated by reduced expression of a subset of M2 effector molecules including arginase 1. Functionally, myeloid Rbpj deficiency impaired M2 effector functions including recruitment of eosinophils and suppression of T cell proliferation. Collectively, we have identified RBP-J as an essential regulator of differentiation and function of alternatively activated macrophages.
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Texto completo:
1
Índice:
WPRIM
Asunto principal:
Farmacología
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Ratones Transgénicos
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Linfocitos T
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Quitina
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Regulación de la Expresión Génica
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Polaridad Celular
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Biología Celular
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Proliferación Celular
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Alergia e Inmunología
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Eosinófilos
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Protein & Cell
Año:
2016
Tipo del documento:
Article