RBP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes

作     者：Julia Foldi Yingli Shang Baohong Zhao Lionel B. Ivashkiv Xiaoyu Hu 

作者机构：Graduate Program in Immunology and Microbial Pathogenesis Weill Cornell Graduate School of Medical Sciences New York NY 10021 USA School of Medicine and Institute for Immunology Tsinghua University Beijing 100084 China Arthritis and Tissue Degeneration Program Hospital for Special Surgery New York NY 10021 USA 

出 版 物：《Protein & Cell》 (蛋白质与细胞（英文版）)

年 卷 期：2016年第7卷第3期

页      面：201-209页

核心收录：

学科分类：0710[理学-生物学] 080503[工学-材料加工工程] 07[理学] 08[工学] 071009[理学-细胞生物学] 09[农学] 0805[工学-材料科学与工程（可授工学、理学学位）] 0901[农学-作物学] 090102[农学-作物遗传育种] 

基　　金：We thank Tasuko Honjo for providing Rbpj^flox/flox mice  Keiko Ozato for providing Ifr8^-/- mice  and Karmen Au for technical assistance. LBI and BZ are supported by the grants from NIH. XH is supported by the National Basic Research Program (973 Program) (No. 2015CB943201)  National Natural Science Foundation of China Young Investigator Award 81422019  and funds from Peking-Tsin- ghua Center of Life Sciences 

主　　题：macrophages RBP-J M2 arginase chitin 

摘      要：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- Jas an essential regulator of differentiation and function of alternatively activated macrophages.