趋化因子
CXCL2型
CCL7型
CCL17型
趋化因子受体
趋化性
CXCL14型
细胞生物学
趋化因子受体
生物
C-C趋化因子受体6型
CXCL1型
化学
免疫学
受体
免疫系统
生物化学
作者
Julie-Randoph Randolph-Habecker,Brian M. Rahill,Beverly Torok‐Storb,Jeffrey Vieira,Pappachan E. Kolattukudy,Brad H. Rovin,Daniel D. Sedmak
出处
期刊:Cytokine
[Elsevier]
日期:2002-07-01
卷期号:19 (1): 37-46
被引量:83
标识
DOI:10.1006/cyto.2002.0874
摘要
We hypothesized that US28, a cytomegalovirus (CMV) CC chemokine receptor homolog, plays a role in modulating the host antiviral defense. Monocyte chemotaxis was induced by supernatants from fibroblasts infected with a US28 deletion mutant of CMV (CMVΔUS28) due to endogenously produced CC chemokines MCP-1 and RANTES. However, these chemokines were sequestered from the supernatants of CMV-infected cells that did express US28. US28 was also capable of sequestering exogenously added RANTES. Surprisingly, cells infected with CMVΔUS28 transcribed and secreted increased levels IL-8, a CXC chemokine, when compared to CMV-infected cells. Finally, because chemokines are potent mediators of immune cell migration through the endothelium, we characterized the CC chemokine binding potential of CMV-infected endothelial cells. We propose that US28 functions as a ‘chemokine sink’ by sequestering endogenously and exogenously produced chemokines and alters the production of the CXC chemokine IL-8, suggesting that CMV could significantly alter the inflammatory milieu surrounding infected cells.
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