The expression of the cytomegalovirus chemokine receptor homolog US28 sequesters biologically active CC chemokines and alters IL-8 production.
The expression of the cytomegalovirus chemokine receptor homolog US28 sequesters biologically active CC chemokines and alters IL-8 production.
复制标题
巨细胞病毒趋化因子受体同源物 US28 的表达会隔离具有生物活性的 CC 趋化因子并改变 IL-8 的产生。
DOI:
10.1006/cyto.2002.0874
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发表时间:
2002
期刊:
影响因子:
3.8
通讯作者:
Sedmak,DanielD
中科院分区:
文献类型:
--
作者:
Randolph-Habecker,Julie-Randoph;Rahill,Brian;Torok-Storb,Beverly;Vieira,Jeffrey;Kolattukudy,PappachanE;Rovin,BradH;Sedmak,DanielD
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.