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Blood, 1 January 2008, Vol. 111, No. 1, pp. 175-182. Prepublished online as a Blood First Edition Paper on September 25, 2007; DOI 10.1182/blood-2007-08-107730. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-08-107730v1 111/1/175    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bolovan-Fritts, C. A. Articles by Spector, S. A. Search for Related Content PubMed PubMed Citation Articles by Bolovan-Fritts, C. A. Articles by Spector, S. A. Related Collections Chemokines, Cytokines, and Interleukins Hemostasis, Thrombosis, and Vascular Biology Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Endothelial damage from cytomegalovirus-specific host immune response can be prevented by targeted disruption of fractalkine-CX3CR1 interaction Cynthia A. Bolovan-Fritts1, and Stephen A. Spector1,3 1 Department of Pediatrics, Division of Infectious Diseases, 2 Center for Molecular Genetics, and 3 Center for AIDS Research, University of California San Diego, La Jolla Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases, including vascular disease and chronic transplant rejection, that involve vascular endothelial damage. We have previously shown that the host CD4+ T-cell response to CMV antigen can produce IFN and TNF at levels sufficient to drive induction of fractalkine, a key marker of inflammation in endothelial cells. We have also observed a major pathogenic effect in which endothelial cell damage and loss follow the induction of frac-talkine and up-regulation of cell adhesion markers in the presence of peripheral blood mononuclear cells (PBMCs) from donors with a high CMV-specific T-cell frequency. In this report, we show that the fractalkine-CX3CR1 interaction resulting in recruitment of natural killer (NK) cells and monocyte-macrophages plays an important role in mediating this endothelial damage. Supportive evidence for frac-talkine's key role is shown by the ability of specific antibody to CX3CR1 to reduce significantly CX3CR1+-bearing cell chemoattraction and to protect against endothelial damage. These findings support CMV as a member of a class of persistent pathogens in which a high T-cell response and chemokine-mediated effects are a risk factor for development of chronic inflammation and endothelial cell injury. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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