ArticlePLoS pathogens2008
The MHV68 M2 protein drives IL-10 dependent B cell proliferation and differentiation.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 67 citations in OpenAlex.
- Model Systems of Gammaherpesvirus Infection, Immunity, and Disease.Journal of medical virology · 2025Review
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment.Nature communications · 2025Article
- Vaccination with a Replication-Dead Murine Gammaherpesvirus Lacking Viral Pathogenesis Genes Inhibits WT Virus Infection.Viruses · 2024Article
- Vaccination with a Replication-Dead Murine Gammaherpesvirus Lacking Viral Pathogenesis Genes Inhibits WT Virus Infection.bioRxiv : the preprint server for biology · 2024Article
- Article
- Characteristics of circulating KSHV-infected viroblasts during active KSHV+ multicentric Castleman disease.Blood advances · 2023Article
- B cell-intrinsic STAT3-mediated support of latency and interferon suppression during murine gammaherpesvirus 68 infection revealed through anbioRxiv : the preprint server for biology · 2023Article
- Epstein-Barr virus, interleukin-10 and multiple sclerosis: A ménage à trois.Frontiers in immunology · 2022Article
- Antibody-independent functions of B cells during viral infections.PLoS pathogens · 2021Review
- Deletion of Murine Gammaherpesvirus GeneJournal of virology · 2020Article
- Review
- Gammaherpesviruses and B Cells: A Relationship That Lasts a Lifetime.Viral immunology · 2020Review
- Regulatory functions of B cells and regulatory plasma cells.Biomedical journal · 2019Review
- Gammaherpesvirus Readthrough Transcription Generates a Long Non-Coding RNA That Is Regulated by Antisense miRNAs and Correlates with Enhanced Lytic Replication In Vivo.Non-coding RNA · 2019Article
- A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes.Nature immunology · 2017Article
- Murine gammaherpesvirus M2 antigen modulates splenic B cell activation and terminal differentiation in vivo.PLoS pathogens · 2017Article
- Article
- Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.Frontiers in microbiology · 2016Review
- M1 of Murine Gamma-Herpesvirus 68 Induces Endoplasmic Reticulum Chaperone Production.Scientific reports · 2015Article
- Does EBV alter the pathogenesis of malaria?Parasite immunology · 2015Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Murine gammaherpesvirus 68 (MHV68) establishes long-term latency in memory B cells similar to the human gammaherpesvirus Epstein Barr Virus (EBV). EBV encodes an interleukin-10 (IL-10) homolog and modulates cellular IL-10 expression; however, the role of IL-10 in the establishment and/or maintenance of chronic EBV infection remains unclear. Notably, MHV68 does not encode an IL-10 homolog, but virus infection has been shown to result in elevated serum IL-10 levels in wild-type mice, and IL-10 deficiency results in decreased establishment of virus latency. Here we show that a unique MHV68 latency-associated gene product, the M2 protein, is required for the elevated serum IL-10 levels observed at 2 weeks post-infection. Furthermore, M2 protein expression in primary murine B cells drives high level IL-10 expression along with increased secretion of IL-2, IL-6, and MIP-1alpha. M2 expression was also shown to significantly augment LPS driven survival and proliferation of primary murine B cells. The latter was dependent on IL-10 expression as demonstrated by the failure of IL10-/- B cells to proliferate in response to M2 protein expression and rescue of M2-associated proliferation by addition of recombinant murine IL-10. M2 protein expression in primary B cells also led to upregulated surface expression of the high affinity IL-2 receptor (CD25) and the activation marker GL7, along with down-regulated surface expression of B220, MHC II, and sIgD. The cells retained CD19 and sIgG expression, suggesting differentiation to a pre-plasma memory B cell phenotype. These observations are consistent with previous analyses of M2-null MHV68 mutants that have suggested a role for the M2 protein in expansion and differentiation of MHV68 latently infected B cells-perhaps facilitating the establishment of virus latency in memory B cells. Thus, while the M2 protein is unique to MHV68, analysis of M2 function has revealed an important role for IL-10 in MHV68 pathogenesis-identifying a strategy that appears to be conserved between at least EBV and MHV68.
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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.