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Front Immunol. 2017 Apr 03;8:373. doi: 10.3389/fimmu.2017.00373. eCollection 2017.

Activation of Adhesion GPCR EMR2/ADGRE2 Induces Macrophage Differentiation and Inflammatory Responses .

Frontiers in immunology

Kuan-Yu I, Yi-Shu Huang, Ching-Hsun Hu, Wen-Yi Tseng, Chia-Hsin Cheng, Martin Stacey, Siamon Gordon, Gin-Wen Chang, Hsi-Hsien Lin

Affiliations

  1. Department of Microbiology and Immunology, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
  2. Division of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital-Keelung, Keelung, Taiwan.
  3. Faculty of Biological Sciences, School of Molecular and Cellular Biology, University of Leeds, Leeds, UK.
  4. Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
  5. Department of Anatomic Pathology, Chang Gung Memorial Hospital-Linkou, Taoyuan, Taiwan.
  6. Chang Gung Immunology Consortium, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan, Taiwan.

PMID: 28421075 PMCID: PMC5376562 DOI: 10.3389/fimmu.2017.00373

Abstract

EMR2/ADGRE2 is a human myeloid-restricted adhesion G protein-coupled receptor critically implicated in vibratory urticaria, a rare type of allergy caused by vibration-induced mast cell activation. In addition, EMR2 is also highly expressed by monocyte/macrophages and has been linked to neutrophil migration and activation. Despite these findings, little is known of EMR2-mediated signaling and its role in myeloid biology. In this report, we show that activation of EMR2

Keywords: EMR2; GPCR; cytokine; inflammation; macrophage; signaling

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