Receptor Expression for IgG Constant Fraction in Human Umbilical Vein Endothelial Cells

Alberto, María Fabiana; Bermejo, Emilse; Lazzari, M.A.

doi:10.1016/s0049-3848(99)00203-0

Cited by 8 publications

(8 citation statements)

References 17 publications

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“…However, no replicative HCV RNA has been detected in endothelial cells in vivo [11] and in our experiments, serum from HCV patients without MC did not induce adhesion molecule expression. Alternatively, HUVEC activation might be due to cryoprecipitate interactions with Fcg receptors (FcgR) [15]. However, in agreement with several other reports [16][17][18], we observed no HUVEC labelling using anti-CD64, anti-CD16 or anti-CD32 mAb.…”

Section: Discussionsupporting

confidence: 89%

Vascular cell adhesion molecule-1 (VCAM-1) plays a central role in the pathogenesis of severe forms of vasculitis due to hepatitis C-associated mixed cryoglobulinemia

Kaplanski

Maisonobe

Marin

et al. 2005

Journal of Hepatology

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Section: Discussionsupporting

confidence: 89%

Vascular cell adhesion molecule-1 (VCAM-1) plays a central role in the pathogenesis of severe forms of vasculitis due to hepatitis C-associated mixed cryoglobulinemia

Kaplanski

Maisonobe

Marin

et al. 2005

Journal of Hepatology

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“…However, there are also reports showing lack of expression of this receptor on HUVEC surface (16,22). Thus, we first set out to determine whether HUVECs express FcgRIIa.…”

Section: Anti-il-8:il-8 Complexes Interact With Fcgriia On Human Endomentioning

confidence: 99%

Anti-Chemokine Autoantibody:Chemokine Immune Complexes Activate Endothelial Cells via IgG Receptors

Krupa¹,

Fudala²,

Stankowska³

et al. 2009

Am J Respir Cell Mol Biol

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“…Whether HUVEC express any FcgR is controversial. This is further complicated by reports that stimulation of HUVEC with cytokines (including TNF-a) or via infection with HSV-1 or CMV upregulates FcgR surface expression [Cines et al, 1982;Friedman, 1989;Favaloro, 1993;MacCormac and Grundy, 1996;Liang et al, 2006], and that even unstimulated HUVEC express surface FcgR [Alberto et al, 2000]. In contrast, there are also reports that none of the three major FcgRs (CD16, CD32, and CD64) are expressed on HUVEC [Sedmak et al, 1991;Groger et al, 1996].…”

Section: Introductionmentioning

confidence: 99%

Primary human endothelial cells support direct but not antibody‐dependent enhancement of dengue viral infection

Arévalo

Simpson-Haidaris

Kou

et al. 2009

Journal of Medical Virology

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Microvascular plasma leakage is the hallmark of dengue hemorrhagic fever and dengue shock syndrome. The precise molecular mechanisms leading to microvascular leakage are yet to be determined, but dengue virus (DENV) infection and consequent endothelial cell death has been suggested as its major cause. However, the extent of endothelial cell permissiveness to DENV infection and the magnitude of cell death following DENV infection are controversial. To clarify this issue, we analyzed the kinetics and consequences of DENV infection of human umbilical vein endothelial cells (HUVEC) using a novel molecularly cloned DENV2-16681 virus. Viral replication was detected as early as 24 hr post-infection by RT-PCR and plaque assays. However, merely 2% of HUVEC were DENV antigen-positive even after 96 hr of infection as measured by the FACS indirect immunofluorescence assays. Unlike monocytes/macrophages, HUVEC did not support antibody dependent enhancement of dengue viral infection due to a lack of FcgammaRI and FcgammaRII. Furthermore, DENV infection did not increase HUVEC apoptosis as compared to mock-infected cells. Because in vitro only a small percentage of endothelial cells were productively infected in vitro with no significant apoptosis occurring in either infected or bystander cells, it would be important to re-examine whether direct dengue viral infection of endothelium is the major cause of the extensive vascular leakage observed in patients with dengue hemorrhagic fever and dengue shock syndrome.

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Receptor Expression for IgG Constant Fraction in Human Umbilical Vein Endothelial Cells

Cited by 8 publications

References 17 publications

Vascular cell adhesion molecule-1 (VCAM-1) plays a central role in the pathogenesis of severe forms of vasculitis due to hepatitis C-associated mixed cryoglobulinemia

Vascular cell adhesion molecule-1 (VCAM-1) plays a central role in the pathogenesis of severe forms of vasculitis due to hepatitis C-associated mixed cryoglobulinemia

Anti-Chemokine Autoantibody:Chemokine Immune Complexes Activate Endothelial Cells via IgG Receptors

Primary human endothelial cells support direct but not antibody‐dependent enhancement of dengue viral infection

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