RBP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes.
10.1007/s13238-016-0248-7
- Author:
Julia FOLDI
1
;
Yingli SHANG
2
;
Baohong ZHAO
3
;
Lionel B IVASHKIV
4
;
Xiaoyu HU
5
Author Information
1. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY, 10021, USA.
2. School of Medicine and Institute for Immunology, Tsinghua University, Beijing, 100084, China.
3. Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY, 10021, USA.
4. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY, 10021, USA. ivashkivl@hss.edu.
5. School of Medicine and Institute for Immunology, Tsinghua University, Beijing, 100084, China. xiaoyuhu@tsinghua.edu.cn.
- Publication Type:Journal Article
- Keywords:
M2;
RBP-J;
arginase;
chitin;
macrophages
- MeSH:
Animals;
Cell Polarity;
drug effects;
genetics;
immunology;
Cell Proliferation;
drug effects;
genetics;
Chitin;
immunology;
pharmacology;
Eosinophils;
cytology;
immunology;
Gene Expression Regulation;
drug effects;
immunology;
Immunoglobulin J Recombination Signal Sequence-Binding Protein;
genetics;
immunology;
Macrophage Activation;
drug effects;
genetics;
Macrophages;
cytology;
immunology;
Mice;
Mice, Transgenic;
T-Lymphocytes;
cytology;
immunology
- From:
Protein & Cell
2016;7(3):201-209
- CountryChina
- Language:English
-
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.
