ArticleJournal of virology2005
Epstein-Barr virus LMP2A alters in vivo and in vitro models of B-cell anergy, but not deletion, in response to autoantigen.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Anti-citrullinated protein antibody response after primary EBV infection in kidney transplant patients.PloS one · 2018Trial
- Epstein-Barr virus as a potentiator of autoimmune diseases.Nature reviews. Rheumatology · 2024Review
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- The impact of Epstein-Barr virus latent membrane protein 2A on the production of B cell activating factor of the tumor necrosis factor family (BAFF), APRIL and their receptors.Immunity, inflammation and disease · 2022Article
- Uncovering early events in primary Epstein-Barr virus infection using a rabbit model.Scientific reports · 2021Article
- Epstein-Barr Virus-Encoded Latent Membrane Protein 2A Downregulates GCNT3 via the TGF-β1/Smad-mTORC1 Signaling Axis.Journal of virology · 2021Article
- Rewiring of B cell receptor signaling by Epstein-Barr virus LMP2A.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Epstein-Barr virus: more than 50 years old and still providing surprises.Nature reviews. Cancer · 2016Review
- Epstein-Barr virus Latent Membrane Protein 2A (LMP2A)-mediated changes in Fas expression and Fas-dependent apoptosis: Role of Lyn/Syk activation.Cellular immunology · 2015Article
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
- EBV Persistence--Introducing the Virus.Current topics in microbiology and immunology · 2015Review
- Epstein-Barr virus, the germinal centre and the development of Hodgkin's lymphoma.The Journal of general virology · 2014Article
- Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Cancer management and research · 2014Review
- The pathogenesis of Epstein-Barr virus persistent infection.Current opinion in virology · 2013Review
- Epstein-Barr virus in systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis—association and causation.Viruses · 2012Review
- Persistence of Epstein-Barr virus in self-reactive memory B cells.Journal of virology · 2012Article
- Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Epstein-Barr virus LMP2A reduces hyperactivation induced by LMP1 to restore normal B cell phenotype in transgenic mice.PLoS pathogens · 2012Article
- Epstein-Barr virus latent membrane protein 2A exacerbates experimental autoimmune encephalomyelitis and enhances antigen presentation function.Scientific reports · 2012Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.