Cytomegalovirus-Induced Effector T Cells Cause Endothelial Cell Damage
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| Published in | Clinical and Vaccine Immunology Vol. 19; no. 5; pp. 772 - 779 |
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| Format | Journal Article |
| Language | English |
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American Society for Microbiology
01.05.2012
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| AbstractList | Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases that involve vascular endothelial cell damage, but definitive proof for a direct cytopathic effect of CMV in these diseases is lacking. CMV infection is associated with a strong increase in both CD4+ and CD8+ T cells with constitutive effector functions that can perpetuate systemic inflammation. We investigated whether CMV-induced immune responses could lead to endothelial damage in humans. We found that terminally differentiated effector CD4+ and CD8+ T cells, formed during primary CMV infection and maintained throughout latency, express high levels of CX3CR1 and CXCR3. The ligands of these receptors, fractalkine and IP-10, respectively, are expressed by activated endothelial cells. Peripheral blood mononuclear cells (PBMC) stimulated with CMV antigen produced soluble factors that stimulated endothelial cells to produce both chemokines. Finally, effector cells migrated in a fractalkine- and IP-10-dependent fashion to activated endothelial cells and induced apoptosis in endothelial cells that were stimulated by supernatant from CMV-activated PBMC. Our findings offer an explanation for the accumulation of highly differentiated T cells near to the endothelium in CMV-infected individuals that may result in endothelial damage. ABSTRACT Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases that involve vascular endothelial cell damage, but definitive proof for a direct cytopathic effect of CMV in these diseases is lacking. CMV infection is associated with a strong increase in both CD4 + and CD8 + T cells with constitutive effector functions that can perpetuate systemic inflammation. We investigated whether CMV-induced immune responses could lead to endothelial damage in humans. We found that terminally differentiated effector CD4 + and CD8 + T cells, formed during primary CMV infection and maintained throughout latency, express high levels of CX3CR1 and CXCR3. The ligands of these receptors, fractalkine and IP-10, respectively, are expressed by activated endothelial cells. Peripheral blood mononuclear cells (PBMC) stimulated with CMV antigen produced soluble factors that stimulated endothelial cells to produce both chemokines. Finally, effector cells migrated in a fractalkine- and IP-10-dependent fashion to activated endothelial cells and induced apoptosis in endothelial cells that were stimulated by supernatant from CMV-activated PBMC. Our findings offer an explanation for the accumulation of highly differentiated T cells near to the endothelium in CMV-infected individuals that may result in endothelial damage. Classifications Services CVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue CVI About CVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy CVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1556-6811 Online ISSN: 1556-679X Copyright © 2014 by the American Society for Microbiology. For an alternate route to CVI .asm.org, visit: CVI Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases that involve vascular endothelial cell damage, but definitive proof for a direct cytopathic effect of CMV in these diseases is lacking. CMV infection is associated with a strong increase in both CD4 + and CD8 + T cells with constitutive effector functions that can perpetuate systemic inflammation. We investigated whether CMV-induced immune responses could lead to endothelial damage in humans. We found that terminally differentiated effector CD4 + and CD8 + T cells, formed during primary CMV infection and maintained throughout latency, express high levels of CX3CR1 and CXCR3. The ligands of these receptors, fractalkine and IP-10, respectively, are expressed by activated endothelial cells. Peripheral blood mononuclear cells (PBMC) stimulated with CMV antigen produced soluble factors that stimulated endothelial cells to produce both chemokines. Finally, effector cells migrated in a fractalkine- and IP-10-dependent fashion to activated endothelial cells and induced apoptosis in endothelial cells that were stimulated by supernatant from CMV-activated PBMC. Our findings offer an explanation for the accumulation of highly differentiated T cells near to the endothelium in CMV-infected individuals that may result in endothelial damage. |
| Author | Si-La Yong Ester B. M. Remmerswaal Pablo J. E. J. van de Berg Ineke J. M. ten Berge René A. W. van Lier |
| Author_xml | – sequence: 1 givenname: Pablo J E J surname: van de Berg fullname: van de Berg, Pablo J E J organization: Department of Experimental Immunology, Academic Medical Center, Amsterdam, Netherlands – sequence: 2 givenname: Si-La surname: Yong fullname: Yong, Si-La – sequence: 3 givenname: Ester B M surname: Remmerswaal fullname: Remmerswaal, Ester B M – sequence: 4 givenname: René A W surname: van Lier fullname: van Lier, René A W – sequence: 5 givenname: Ineke J M surname: ten Berge fullname: ten Berge, Ineke J M |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22398244$$D View this record in MEDLINE/PubMed |
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Reddit... Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases that involve vascular endothelial cell damage, but definitive proof for a direct... ABSTRACT Human cytomegalovirus (CMV) infection has been linked to inflammatory diseases that involve vascular endothelial cell damage, but definitive proof for... |
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| SubjectTerms | Apoptosis CD4 antigen CD4-Positive T-Lymphocytes - immunology CD8 antigen CD8-Positive T-Lymphocytes - immunology Chemokine CX3CL1 - biosynthesis Chemokine CXCL10 - biosynthesis Chemokines Clinical Immunology CX3C Chemokine Receptor 1 CX3CR1 protein CXCR3 protein Cytokines - secretion Cytomegalovirus - immunology Cytomegalovirus - pathogenicity Cytomegalovirus Infections - immunology Cytomegalovirus Infections - pathology Effector cells Endothelial cells Endothelial Cells - immunology Endothelial Cells - virology Endothelium Fractalkine Gene Expression Human cytomegalovirus Humans Infection Inflammatory diseases IP-10 protein Leukocytes, Mononuclear - immunology Lymphocytes T Peripheral blood mononuclear cells Receptors, Chemokine - biosynthesis Receptors, CXCR3 - biosynthesis |
| Title | Cytomegalovirus-Induced Effector T Cells Cause Endothelial Cell Damage |
| URI | http://cvi.asm.org/content/19/5/772.abstract https://www.ncbi.nlm.nih.gov/pubmed/22398244 https://search.proquest.com/docview/1010231373 https://search.proquest.com/docview/1020840043 https://pubmed.ncbi.nlm.nih.gov/PMC3346330 |
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