RBP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes. Issue 3 (13th February 2016)

• Record Type: Journal Article
• Authors: Foldi, Julia; Shang, Yingli; Zhao, Baohong; Ivashkiv, Lionel B; Hu, Xiaoyu
• Is Part Of: Protein & cell. Volume 7:Issue 3(2016)
• Page Start: 201
• Page End: 209
• Publication Date: 2016-02-13
• Subjects: macrophages -- RBP-J -- M2 -- arginase -- chitin; Proteins -- Periodicals; Cells -- Periodicals; Cytology -- Periodicals; 572.6
• DOI: 10.1007/s13238-016-0248-7
• Languages: English
• ISSNs: 1674-800X

Abstract

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.