Abstract:
:A significant percentage of the population latently harbors Epstein-Barr virus (EBV) in B cells. One EBV-encoded protein, latent membrane protein 2A (LMP2A), is expressed in tissue culture models of EBV latent infection, in human infections, and in many of the EBV-associated proliferative disorders. LMP2A constitutively activates proteins involved in the B-cell receptor (BCR) signal transduction cascade and inhibits the antigen-induced activation of these proteins. In the present study, we investigated whether LMP2A alters B-cell receptor signaling in primary B cells in vivo and in vitro. LMP2A does not inhibit antigen-induced tolerance in response to strong stimuli in an in vivo tolerance model in which B cells are reactive to self-antigen. In contrast, LMP2A bypasses anergy induction in response to low levels of soluble hen egg lysozyme (HEL) both in vivo and in vitro as determined by the ability of LMP2A-expressing HEL-specific B cells to proliferate and induce NF-kappaB nuclear translocation after exposure to low levels of antigen. Furthermore, LMP2A induces NF-kappaB nuclear translocation independent of BCR cross-linking. Since NF-kappaB is required to bypass tolerance induction, this LMP2A-dependent NF-kappaB activation may complete the tolerogenic signal induced by low levels of soluble HEL. Overall, the findings suggest that LMP2A may not inhibit BCR-induced signals under all conditions as previously suggested by studies with EBV immortalized B cells.
journal_name
J Viroljournal_title
Journal of virologyauthors
Swanson-Mungerson MA,Caldwell RG,Bultema R,Longnecker Rdoi
10.1128/JVI.79.12.7355-7362.2005subject
Has Abstractpub_date
2005-06-01 00:00:00pages
7355-62issue
12eissn
0022-538Xissn
1098-5514pii
79/12/7355journal_volume
79pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 临床试验,杂志文章
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更新日期:1994-12-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2007-04-01 00:00:00