Selective migration of highly differentiated primed T cells, defined by low expression of CD45RB, across human umbilical vein endothelial cells: effects of viral infection on transmigration

Borthwick, Nicola; Akbar, Arne N.; MacCormac, Luci P.; Lowdell, MW; Craigen, J L; Hassan, Imad; Grundy, Jane E.; Salmon, Mike; Yong, Kwee

doi:10.1046/j.1365-2567.1997.00154.x

Cited by 31 publications

(24 citation statements)

References 32 publications

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“…Recent reports suggest that RANTES and lymphotactin enhance movement of lymphocytes across HUVECs (8), while other chemokines, such as MIP-1␣, MIP-1␤, MCP-1, and IL-8, did not demonstrate a selective ability to induce lymphocyte migration across HUVECs (8) and were not regulated in our system (Fig. 4).…”

Section: Discussionmentioning

confidence: 50%

Viral Regulation of RANTES Expression during Human Cytomegalovirus Infection of Endothelial Cells

Schroeder

Worthen

2001

J Virol

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Section: Discussionmentioning

confidence: 50%

Viral Regulation of RANTES Expression during Human Cytomegalovirus Infection of Endothelial Cells

Schroeder

Worthen

2001

J Virol

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“…Thus lymphotactin was able to chemoattract murine lymphocytes (29,34) and humane lymphocytes from peripheral blood (26,35,36,38). Therefore it was unexpected that we found vCCL3 and XCL1 unable to chemoattract human PBLs.…”

Section: Discussionmentioning

confidence: 78%

Kaposi Sarcoma-associated Herpes Virus Targets the Lymphotactin Receptor with Both a Broad Spectrum Antagonist vCCL2 and a Highly Selective and Potent Agonist vCCL3

Lüttichau¹,

Johnsen²,

Jurlander

et al. 2007

Journal of Biological Chemistry

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Large DNA viruses such as herpesvirus and poxvirus encode proteins that target and exploit the chemokine system of their host. These proteins have the potential to block or change the orchestrated recruitment of leukocytes to sites of viral infection. The genome of Kaposi sarcoma-associated herpes virus (KSHV) encodes three chemokine-like proteins named vCCL1, vCCL2, and vCCL3. In this study vCCL3 was probed in parallel with vCCL1 and vCCL2 against a panel of the 18 classified human chemokine receptors. In calcium mobilization assays vCCL1 acted as a selective CCR8 agonist, whereas vCCL2 was found to act as a broad spectrum chemokine antagonist of human chemokine receptors, including the lymphotactin receptor. In contrast vCCL3 was found to be a highly selective agonist for the human lymphotactin receptor XCR1. The potency of vCCL3 was found to be 10-fold higher than the endogenous human XCL1 chemokine in respect to phosphatidylinositol turnover and calcium mobilization as well as chemotaxis. High expression of XCR1 was found in placenta and neutrophils by real-time PCR. These data are consistent with reports of different expression profiles for vCCL2 and vCCL3 during the life cycle of KSHV, indicate a novel, sophisticated exploitation by the virus of specifically the lymphotactin receptor by both agonist and antagonist mechanisms, and suggest a unique physiological importance of this (somewhat overlooked) chemokine receptor.

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“…This strategy would allow for the spread of the virus from the blood into the surrounding tissue, but to be effective, the infected endothelium must pass the virus to naïve monocytes. The transfer of the virus between different cell types is supported by studies showing that endothelial cell-monocyte interactions allow for the spread of the virus from one cell type to another (9,32,33,96). Here we describe a potential mechanism for the role infected endothelial cells play in viral pathogenesis.…”

mentioning

confidence: 81%

Human Cytomegalovirus (HCMV) Infection of Endothelial Cells Promotes Naïve Monocyte Extravasation and Transfer of Productive Virus To Enhance Hematogenous Dissemination of HCMV

Bentz

Jarquin-Pardo

Chan

et al. 2006

J Virol

120

124

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Human cytomegalovirus (HCMV) pathogenesis is dependent on the hematogenous spread of the virus to host tissue. While data suggest that infected monocytes are required for viral dissemination from the blood to the host organs, infected endothelial cells are also thought to contribute to this key step in viral pathogenesis. We show here that HCMV infection of endothelial cells increased the recruitment and transendothelial migration of monocytes. Infection of endothelial cells promoted the increased surface expression of cell adhesion molecules (intercellular cell adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and platelet endothelial cell adhesion molecule 1), which were necessary for the recruitment of naïve monocytes to the apical surface of the endothelium and for the migration of these monocytes through the endothelial cell layer. As a mechanism to account for the increased monocyte migration, we showed that HCMV infection of endothelial cells increased the permeability of the endothelium. The cellular changes contributing to the increased permeability and increased naïve monocyte transendothelial migration include the disruption of actin stress fiber formation and the decreased expression of lateral junction proteins (occludin and vascular endothelial cadherin). Finally, we showed that the migrating monocytes were productively infected with the virus, documenting that the virus was transferred to the migrating monocyte during passage through the lateral junctions. Together, our results provide evidence for an active role of the infected endothelium in HCMV dissemination and pathogenesis.Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes a life-long persistent infection (10). In immunocompromised individuals, such as AIDS patients, neonates, and transplant recipients, HCMV infection is associated with significant morbidity and mortality (13,38,56,87). In immunocompetent hosts, HCMV infection is generally asymptomatic, although it can cause mononucleosis (40) and is associated with chronic inflammatory diseases, such as the cardiovascular diseases atherosclerosis and coronary restenosis (1,19,35,46,51,57,59,86,90,107).HCMV pathogenesis is a direct result of viral spread to host organs and the subsequent infection of those organ systems (6,44,54,83). Systemic spread occurs during both asymptomatic and symptomatic infections (93) and is required for HCMV persistence in the host (83). During primary infection, the virus spreads from the initial site of infection to the peripheral blood and then to host organ tissue (6,54,83). In healthy hosts, infection of these organ systems allows for the establishment of the viral persistence needed for viral survival in the infected host and in the general population. In contrast, in immunocompromised hosts, because of the absence of a functional immune response, this same strategy of viral spread would lead to the overt organ disease seen in these individuals (83).The mechanisms of HCMV dissemination remain unclear; however, cells of the ...

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Selective migration of highly differentiated primed T cells, defined by low expression of CD45RB, across human umbilical vein endothelial cells: effects of viral infection on transmigration

Cited by 31 publications

References 32 publications

Viral Regulation of RANTES Expression during Human Cytomegalovirus Infection of Endothelial Cells

Viral Regulation of RANTES Expression during Human Cytomegalovirus Infection of Endothelial Cells

Kaposi Sarcoma-associated Herpes Virus Targets the Lymphotactin Receptor with Both a Broad Spectrum Antagonist vCCL2 and a Highly Selective and Potent Agonist vCCL3

Human Cytomegalovirus (HCMV) Infection of Endothelial Cells Promotes Naïve Monocyte Extravasation and Transfer of Productive Virus To Enhance Hematogenous Dissemination of HCMV

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