期刊
CELL REPORTS
卷 15, 期 7, 页码 1542-1553出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.04.042
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资金
- European Research Council under the European Union's Seventh Framework Programme (FP)/ERC Grant [320473-BacNK]
- I-CORE Program of the Planning and Budgeting Committee
- Israel Science Foundation [275/13]
- I-Core on Chromatin and RNA in Gene Regulation
- GIF foundation
- Lewis family foundation
- ICRF professorship grant
- Israeli Science Foundation
- Helmholtz Israel grant
- Rosetrees Trust
- Israeli Ministry of Health [10998]
- European Union [316655]
- Samueli Institute Brain Mind & Healing Center, under US Army Medical Research and Materiel Command (USAMRAA award) [W81XWH-10-1-0938]
HCMV is a highly sophisticated virus that has developed various mechanisms for immune evasion and viral dissemination throughout the body (partially mediated by neutrophils). NK cells play an important role in elimination of HCMV-infected cells. Both neutrophils and NK cells utilize similar sets of chemokine receptors to traffic, to and from, various organs. However, the mechanisms by which HCMV attracts neutrophils and not NK cells are largely unknown. Here, we show a unique viral protein, vCXCL1, which targets three chemokine receptors: CXCR1 and CXCR2 expressed on neutrophils and CXCR1 and CX3CR1 expressed on NK cells. Although vCXCL1 attracted both cell types, neutrophils migrated faster and more efficiently than NK cells through the binding of CXCR2. Therefore, we propose that HCMV has developed vCXCL1 to orchestrate its rapid systemic dissemination through preferential attraction of neutrophils and uses alternative mechanisms to counteract the later attraction of NK cells.
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