1887

Abstract

In cell lines, the Epstein–Barr virus (EBV)-encoded protein latent membrane protein 2A (LMP2A) protects B-cells from apoptosis by blocking B-cell receptor (BCR) signalling. However, EBV-infected B-cells are extremely different from cell lines. This study used a murine transgenic model in which B-cells express LMP2A and a BCR specific for hen egg lysozyme to determine whether LMP2A protects resting and antigen-activated B-cells from apoptosis. LMP2A allows BCR signal transduction and induces constitutive activation of NF-B to increase Bcl-2 levels that afford LMP2A-mediated protection from apoptosis in the absence or presence of antigen. In contrast, low levels of NF-B inhibitor only affected Bcl-2 and Bcl-xL levels and increased apoptosis in LMP2A-negative B-cells after BCR cross-linking. These data suggest that LMP2A uniquely makes resting B-cells sensitive to NF-B inhibition and apoptosis and suggest that NF-B may be a novel target to eradicate latently EBV-infected B-cells.

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2010-09-01
2024-04-19
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vol. , part 9, pp. 2197–2202

Bcl-2 and Bcl-xL levels in wild-type and LMP2A-Tg B-cells.

Annexin V staining of HEL-Tg and LMP2A/HEL-Tg B-cells.

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