CD312, the human adhesion-GPCR EMR2, is differentially expressed during differentiation, maturation, and activation of myeloid cells

被引:41
作者
Chang, Gin-Wen
Davies, John Q.
Stacey, Martin
Yona, Simon
Bowdish, Dawn M. E.
Hamann, Jorg
Chen, Tse-Ching
Lin, Chun-Yen
Gordon, Siamon
Lin, Hsi-Hsien
机构
[1] Chang Gung Univ, Dept Microbiol & Immunol, Tao Yuan, Taiwan
[2] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England
[3] Univ Amsterdam, Acad Med Ctr, Dept Expt Immunol, NL-1105 AZ Amsterdam, Netherlands
[4] Chang Gung Mem Hosp, Dept Pathol, Tao Yuan, Taiwan
[5] Chang Gung Mem Hosp, Dept Hepatogastroenterol, Tao Yuan, Taiwan
基金
英国医学研究理事会;
关键词
adhesion-GPCR; EGF-TM7; EMR2; myeloid cell;
D O I
10.1016/j.bbrc.2006.11.148
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
EMR2/CD312 is a member of the adhesion-GPCR family that contains extracellular EGF-like domains. Previously it has been shown to interact with chondroitin sulphate glycosatninoglycans in an isoform-specific manner. Although EMR2 expression has been found to be restricted to human myeloid cells, its expression profile has not yet been systemically characterized. In this report, we show that EMR2 receptor expression is up-regulated during differentiation and maturation of macrophages, and is conversely down-regulated during dendritic cell maturation. We also demonstrate that EMR2 receptor alternative splicing and glycosylation is regulated during myeloid differentiation. In monocytes and macrophages, EMR2 can be specifically up-regulated by LPS and IL-10 via an IL-10-mediated pathway. In inflamed tissues, EMR2 is detected in subpopulations of myeloid cells including macrophages and neutrophils. The results presented here further support the idea that EMR2 plays a role in the migration and adhesion of myeloid cells during cell differentiation, maturation, and activation. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:133 / 138
页数:6
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