Epstein-Barr Virus LMP2A Enhances B-Cell Responses In Vivo and In Vitro

Swanson‐Mungerson, Michelle; Bultema, Rebecca; Longnecker, Richard

doi:10.1128/jvi.00433-06

Cited by 30 publications

(37 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, B cells from both LMP2A CD19 and LMP2A AID mice displayed significantly accelerated in vitro differentiation into ASCs when stimulated with anti-CD40 antibody or sCD40L in combination with IL-4. These results are consistent with the reports that LMP2A expression facilitates plasma cell differentiation in vitro and in vivo in response to CD40 stimulation or Toll-like receptor agonists (40,41). These findings strongly suggest that LMP2A affects BCR signals as well as CD40 signals.…”

Section: Discussionsupporting

confidence: 83%

Evasion of affinity-based selection in germinal centers by Epstein–Barr virus LMP2A

Minamitani

Yasui

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 83%

Evasion of affinity-based selection in germinal centers by Epstein–Barr virus LMP2A

Minamitani

Yasui

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

“…It is difficult to conceive how this augmentation could result in more stringent selection; however, it could lead to more rounds of expansion and survival as suggested by an LMP2a/hen egg lysosome transgenic mouse model (25). Because LMP2a alone cannot drive proliferation, Ag recognition would be necessary to initiate the GC reaction; then LMP2a could cooperate with Ag to allow the survival of latently infected B cells in the GC even if they generated a suboptimal BCR signal (10,13,26). Alternatively, LMP1 is known to provide a constitutive T H signal, and it is known that extended Th signaling preferentially drives GC B cells to become memory rather than plasma cells (27).…”

Section: Discussionmentioning

confidence: 99%

Influence of EBV on the Peripheral Blood Memory B Cell Compartment

Souza

Stollar

Sullivan

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

Peripheral blood memory B cells latently infected with EBV bear somatic mutations and are typically isotype switched consistent with being classical Ag-selected memory B cells. In this work, we performed a comparative analysis of the expressed Ig genes between large sets of EBV-infected and uninfected peripheral blood B cells, isolated from the same infectious mononucleosis patients, to determine whether differences exist that could reveal the influence of EBV on the production and maintenance of these cells. We observed that EBV+ cells on average accumulated more somatic hypermutations than EBV− cells. In addition, they had more replacement mutations and a higher replacement-silent ratio of mutations in their CDRs. We also found that EBV occupies a skewed niche within the memory compartment, due to its exclusion from the CD27+IgD+IgM+ subset, but this skewing does not affect the overall structure of the compartment. These results indicate that EBV impacts the mutation and selection process of infected cells but that once they enter memory they cannot be distinguished from uninfected cells by host homeostasis mechanisms.

show abstract

“…LMP1 functions as a constitutively active, ligand-independent tumor necrosis factor receptor to activate the NF-B, MAPK, PI3K, and JAK3/STAT pathways (16,18,21,27,45) and provide signals equivalent to those induced by CD40 ligand (35,69). The LMP2 latency membrane protein is not essential for in vitro B-cell immortalization (60) but provides important in vivo survival signals that mimic those arising from B-cell receptor activation (55,63). The recent recognition that TLR signaling may serve as a third signal for optimal B-cell activation, along with antigen binding to the B-cell receptor and CD40 stimulation (56), led us to investigate interactions between the EBV and TLR pathways.…”

mentioning

confidence: 99%