B Cell Phenotype-dependent Expression of the Epstein-Barr Virus Nuclear Antigens EBNA-2 to EBNA-6: Studies with Somatic Cell Hybrids

Contreras-Brodin, Bertha A.; Anvret, Maria; Imreh, Stefan; Altıok, Ender; Klein, George; Masucci, Maria G.

doi:10.1099/0022-1317-72-12-3025

Cited by 46 publications

(35 citation statements)

References 53 publications

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“…Interestingly, this case was negative for EBV. The lack of EBV-mediated down-regulation of BCL-6 expression and promotion of further B-cell maturation Contreras-Broding et al, 1991;Rowe et al, 1994;Sample et al, 1991;Schaefer et al, 1991) could have facilitated persistence of the BCL-6 expression in this case. …”

Section: Paessler Et Almentioning

confidence: 90%

“…EBV seems, indeed, to play a major role in induction of the post-germinal center cell phenotype. Previous studies have shown that LMP-1, which is one of the key proteins responsible for the EBV-mediated cell transformation (Tanner and Alfieri, 2001;Tao and Wasik, 2001), is able to down-regulate expression of BCL-6 in germinal center B cells and drive their maturation to the post-germinal center stage Contreras-Broding et al, 1991;Rowe et al, 1994;Sample et al, 1991;Schaefer et al, 1991). Accordingly, the post-germinal center cell phenotype is not unique to the EBV ϩ B-cell PTLDs but is also present in the EBV ϩ AIDS-related non-Hodgkin's lymphomas (Carbone et al, 1998a).…”

Section: Paessler Et Almentioning

confidence: 99%

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Expression of SHP-1 Phosphatase Indicates Post-Germinal Center Cell Derivation of B-Cell Posttransplant Lymphoproliferative Disorders

Paessler

Kossev

Tsai

et al. 2002

Laboratory Investigation

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SUMMARY: SHP-1 tyrosine phosphatase acts as a negative regulator of signaling by receptors for growth factors, cytokines, and chemokines and by receptors involved in immune response. Our recent study showed that SHP-1 is tightly regulated at various stages of B-cell differentiation and is expressed in the mantle and marginal zones, interfollicular B cells, and plasma cells, whereas it is nondetectable in germinal center cells. In this study we evaluated expression of SHP-1 in vitro and in vivo in nine cell lines representing three different types of EBV ϩ B-cell populations closely resembling or derived from posttransplant lymphoproliferative disorders (PTLDs). Furthermore, we examined tissue samples from 58 patients with B-cell PTLDs, both EBV ϩ (85% of the cases analyzed) and EBV Ϫ (15%). SHP-1 protein was strongly expressed in all cell lines and PTLD cases. In addition, the PTLD cases were essentially negative for germinal center B-cell markers: none expressed CD10 and only one expressed BCL-6. More than 40% expressed a late post-germinal B-cell marker, CD138. The universal expression of SHP-1, lack of expression of CD10 and BCL-6, and frequent expression of CD138 suggest that PTLDs are derived from post-germinal center B cells regardless of the EBV cell infection status. Based on the immunophenotype, B-cell PTLDs could be divided into two broad categories corresponding to the early (CD10 Ϫ /BCL-6 Ϫ /SHP-1 ϩ /CD138 Ϫ ) and late (CD10 Ϫ /BCL-6 Ϫ /SHP-1 ϩ /CD138 ϩ ) postgerminal center cells. By being expressed earlier, SHP-1 is a more sensitive marker of post-germinal center B cells than CD138, which is seen on the terminally differentiated immunoblasts and plasma cells. (Lab Invest 2002, 82:1599 -1606.

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Section: Paessler Et Almentioning

confidence: 90%

Section: Paessler Et Almentioning

confidence: 99%

Expression of SHP-1 Phosphatase Indicates Post-Germinal Center Cell Derivation of B-Cell Posttransplant Lymphoproliferative Disorders

Paessler

Kossev

Tsai

et al. 2002

Laboratory Investigation

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“…First, we examined the endogenous levels of Twist protein in a set of EBV-infected cell lines. KH-1 and KH-2 are type II latently infected adherent cell lines derived by fusion of an EBV-infected lymphoblastoid suspension cell line, KR4, with adherent HeLa cells (40). The expression level of Twist protein is significantly higher in KR4, KH-1, and KH-2 cells than in the EBV-negative parental HeLa cells (Fig.…”

Section: Lmp1 Induces Emtmentioning

confidence: 94%

Twist and Epithelial-Mesenchymal Transition Are Induced by the EBV Oncoprotein Latent Membrane Protein 1 and Are Associated with Metastatic Nasopharyngeal Carcinoma

et al. 2007

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Nasopharyngeal carcinoma (NPC), an EBV-associated malignancy, is highly metastatic compared with other head and neck tumors, perhaps because of its viral link. Here, we show that the principal EBV oncoprotein, latent membrane protein 1 (LMP1), induces epithelial-mesenchymal transition (EMT) via Twist, a master transcriptional regulator in embryogenesis and newly implicated in metastasis, which, in turn, are likely to contribute to the highly metastatic character of NPC. LMP1 could induce EMT and its associated cell motility and invasiveness in a cell culture model, whereas expression of Twist small interfering RNA reversed LMP1-induced EMT. In diverse EBV-infected cell lines, expression of Twist correlates with expression of LMP1. Dominant-negative LMP1 could suppress Twist expression in EBV-positive cells, whereas LMP1 could induce Twist in EBV-negative nasopharyngeal cells. LMP1 signals through the nuclear factor-KB pathway, and an IKB superrepressor inhibited induction of Twist by LMP1. Finally, in human NPC tissues, expression of Twist and LMP1 is directly correlated and expression of Twist is associated with metastasis clinically. These results suggest that induction of Twist by a human viral oncoprotein LMP1 directly contributes to the metastatic nature of NPC. [Cancer Res 2007;67(5):1970-8]

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“…Concomitantly, they lost EBNA-2 expression. On the other hand, the two LCL-HeLa hybrids maintained the LMP-1 expression (Contreras-Brodin et al, 1991). The downregulation of EBNA-2 in these hybrids occurred at the transcriptional level, as detected by the lack of Cp-initiated transcripts (Altiok et al, 1992).…”

Section: Hodgkin Lymphomamentioning

confidence: 94%

“…These proteins are known to activate the viral-Wp and Cp promoters (Contreras-Brodin et al, 1996;Tierney et al, 2000) and therefore required to generate the giant mRNA from which all six EBNA messages are spliced in type III latency. The need for B-cell-specific factors for type III latent gene expression was first demonstrated in work with somatic cell hybrids (Contreras-Brodin et al, 1991). Whenever an EBV-carrying LCL or the Type III BL line Raji were fused with non-B-cell partners such as HeLa (human cervical carcinoma) or A9HT (mouse fibrosarcoma), respectively, the B-cell phenotype eclipsed.…”

Section: Hodgkin Lymphomamentioning

confidence: 99%

Epstein–Barr virus infection in humans: from harmless to life endangering virus–lymphocyte interactions

2007

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B Cell Phenotype-dependent Expression of the Epstein-Barr Virus Nuclear Antigens EBNA-2 to EBNA-6: Studies with Somatic Cell Hybrids

Cited by 46 publications

References 53 publications

Expression of SHP-1 Phosphatase Indicates Post-Germinal Center Cell Derivation of B-Cell Posttransplant Lymphoproliferative Disorders

Expression of SHP-1 Phosphatase Indicates Post-Germinal Center Cell Derivation of B-Cell Posttransplant Lymphoproliferative Disorders

Twist and Epithelial-Mesenchymal Transition Are Induced by the EBV Oncoprotein Latent Membrane Protein 1 and Are Associated with Metastatic Nasopharyngeal Carcinoma

Epstein–Barr virus infection in humans: from harmless to life endangering virus–lymphocyte interactions

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