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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1857-1863. Prepublished online as a Blood First Edition Paper on May 22, 2007; DOI 10.1182/blood-2007-03-078881. This Article Full Text Full Text (PDF) Supplemental Methods All Versions of this Article: blood-2007-03-078881v1 110/6/1857    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 HighWire 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 Hemostasis, Thrombosis, and Vascular Biology Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY High T-cell response to human cytomegalovirus induces chemokine-mediated endothelial cell damage Cynthia A. Bolovan-Fritts1, Rodney N. Trout1, 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 that involve vascular endothelial damage, including vascular disease and chronic transplant rejection. We previously reported that the host CD4+ T-cell response to CMV antigen presented by endothelial cells can produce interferon- and tumor necrosis factor- at levels sufficient to drive induction of fractalkine, a key marker of inflammation, in endothelial cells. In this work, we report that donors with high frequencies of antigen-specific T cells to CMV (high responders) induce higher levels of activation-associated chemokines such as fractalkine, RANTES (regulated on activation, normal T cell expressed and secreted), and macrophage inflammatory protein-1ß, together with cell-adhesion markers in endothelial cells compared with donors with low levels of CMV-specific T cells (low responders). High-responder cultures had higher levels of leukocyte recruitment and adherence to the endothelial monolayers associated with progressive damage and loss of the endothelial cells. These processes that led to endothelial destruction only required viral antigen and did not require infectious virus. Our findings further support that CMV may represent one member of a class of persistent pathogens in which a high antigen-specific T-cell response defines an important risk factor for development of chronic inflammation and endothelial cell injury. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. Bolovan-Fritts and S. A. Spector Endothelial damage from cytomegalovirus-specific host immune response can be prevented by targeted disruption of fractalkine-CX3CR1 interaction Blood, January 1, 2008; 111(1): 175 - 182. [Abstract] [Full Text] [PDF]

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