Binding of the endogenously expressed Epstein-Barr virus (EBV) envelope glycoprotein gp350 with the viral receptor masks the major EBV-neutralizing epitope and affects gp350-specific ADCC

Khyatti, Meriem; Ahmad, Ali; Blagdon, Marie; Frade, Raymond; Menezes, José

doi:10.1002/jlb.64.2.192

Cited by 9 publications

(5 citation statements)

References 37 publications

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“…Similarly, NK cell degranulation as a measure of NK-inducing Ab activity, was substantially decreased during the first year of infection compared to what had been previously described by others [12,13]. However, in line with previously published observations, gp350/220-specific Abs in individuals with chronic EBV infection were capable of engaging NK cell functions [43,44], although not as efficient as influenza HA1-specific antibodies. Therefore, the non-neutralizing Ab response to EBV is characterized by an immediate induction of ADCD and ADNP by p18-specific Abs during the acute phase of infection.…”

Section: Plos Pathogenssupporting

confidence: 84%

Evolution of functional antibodies following acute Epstein-Barr virus infection

et al. 2022

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While Epstein-Barr virus causes mostly asymptomatic infection, associated malignancies, and autoimmune and lymphoproliferative diseases occur. To dissect the evolution of humoral immune responses over the course of EBV infection and to gain a better understanding of the potential contribution of antibody (Ab) function to viral control, we comprehensively profiled Ab specificities and Fc-functionalities using systems serology and VirScan. Ab functions against two early (p18 and p47/54) and two latent (gp350/220 and EBNA-1) EBV proteins were overall modest and/or short-lived, differing from humoral responses induced during acute infection by other viruses such as HIV. In the first year post infection, only p18 elicited robust IgM-driven complement deposition and IgG-driven neutrophil phagocytosis while responses against EBNA-1 were largely Fc-functionally silent and only matured during chronic infection to drive phagocytosis. In contrast, Abs against Influenza virus readily mediated broad Fc-activity in all participants. These data suggest that EBV evades the induction of robust Fc-functional Abs, potentially due to the virus’ life cycle, switching from lytic to latent stages during infection.

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Section: Plos Pathogenssupporting

confidence: 84%

Evolution of functional antibodies following acute Epstein-Barr virus infection

et al. 2022

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“…This observation suggests the presence of gp350 on the surface of LCL1 exosomes and that this EBV glycoprotein, and not CD23, mediates the exosome binding. As a control, we also added a nonneutralizing anti-gp350 mAb (2L10) (29), which did not block exosome binding (data not shown), reinforcing the notion of a specific blocking of gp350 via the neutralizing mAb (72A1).…”

Section: Gp350 On Lcl1 Exosomes Mediates the Binding To B Cellsmentioning

confidence: 54%

Exosomes Containing Glycoprotein 350 Released by EBV-Transformed B Cells Selectively Target B Cells through CD21 and Block EBV Infection In Vitro

Vallhov

Gutzeit

Johansson

et al. 2011

The Journal of Immunology

122

113

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Exosomes are nano-sized membrane vesicles released from a wide variety of cells, formed in endosomes by inward budding of the endosomal limiting membrane. They have immune stimulatory-, inhibitory-, or tolerance-inducing effects, depending on their cellular origin, which is why they are investigated for use in vaccine and immune therapeutic strategies. In this study, we explored whether exosomes of different origins and functions can selectively target different immune cells in human peripheral blood. Flow cytometry, confocal laser scanning microscopy, and multispectral imaging flow cytometry (ImageStream) revealed that exosomes derived from human monocyte-derived dendritic cells and breast milk preferably associated with monocytes. In contrast, exosomes from an EBV-transformed B cell line (LCL1) preferentially targeted B cells. This was not observed for an EBV− B cell line (BJAB). Electron microscopy, size-distribution analysis (NanoSight), and a cord blood transformation assay excluded the presence of virions in our LCL1 exosome preparations. The interaction between LCL1-derived exosomes and peripheral blood B cells could be blocked efficiently by anti-CD21 or anti-gp350, indicating an interaction between CD21 on B cells and the EBV glycoprotein gp350 on exosomes. The targeting of LCL1-derived exosomes through gp350–CD21 interaction strongly inhibited EBV infection in B cells isolated from umbilical cord blood, suggesting a protective role for exosomes in regulating EBV infection. Our finding also suggests that exosome-based vaccines can be engineered for specific B cell targeting by inducing gp350 expression.

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“…In order to determine whether thrombin treatment of the human tumor cells had any effect on apoptosis‐related proteins p53, bcl‐2 or p21, Western blots were performed as described earlier (Khyatti et al, 1998). Briefly, 5×10 6 cells (with or without incubation with thrombin) were lysed 24 to 30 hours later in 500 μl of the lysis buffer containing Tris HCl (pH 6.8; 10 mM), and SDS (2%), and sonicated for 15 seconds on ice.…”

Section: Methodsmentioning

confidence: 99%

Thrombin induces apoptosis in human tumor cells

Ahmad

Knafo

et al. 2000

Int. J. Cancer

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Thrombin is a serine protease that is produced during the coagulation process and plays an essential role for hemostasis, thrombosis and wound healing. It is a potent activator of platelets, induces proliferation of a wide variety of normal and malignant human cells, and enhances their invasiveness and metastatic potential. We studied the effect of thrombin on the proliferation of a wide variety of human tumor cells and report here that, at low concentrations, thrombin induces proliferation of these cells. However, at higher concentrations, thrombin inhibited their proliferation. We show that this inhibition of cell proliferation was due to apoptosis of the tumor cells. The thrombin‐mediated apoptosis was inhibited significantly by its specific inhibitor, hirudin. Furthermore, no consistent pattern of induction and/or modulation of p53, p21 and bcl‐2 was observed in the thrombin‐mediated apoptosis. To our knowledge, this is the first report to describe the pro‐apoptotic effects of thrombin on human tumor cells and may have implications for chemotherapy in cancer patients and for the pathogenesis of AIDS as well. Int. J. Cancer 87:707–715, 2000. © 2000 Wiley‐Liss, Inc.

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Binding of the endogenously expressed Epstein-Barr virus (EBV) envelope glycoprotein gp350 with the viral receptor masks the major EBV-neutralizing epitope and affects gp350-specific ADCC

Cited by 9 publications

References 37 publications

Evolution of functional antibodies following acute Epstein-Barr virus infection

Evolution of functional antibodies following acute Epstein-Barr virus infection

Exosomes Containing Glycoprotein 350 Released by EBV-Transformed B Cells Selectively Target B Cells through CD21 and Block EBV Infection In Vitro

Thrombin induces apoptosis in human tumor cells

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