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B-lymphocyte-induced maturation protein 1 (BLIMP1) exists as two major isoforms, α and β, which arise from alternate promoters. Inactivation of the full length BLIMP1α isoform is thought to contribute to B cell lymphomagenesis by blocking post-germinal centre (GC) B cell differentiation. In contrast, the shorter β isoform is functionally impaired and over-expressed in several haematological malignancies, including diffuse large B cell lymphomas (DLBCL). We have studied the influence on BLIMP1β expression of the Epstein-Barr virus (EBV), a human herpesvirus that is implicated in the pathogenesis of several GC-derived lymphomas, including a subset of DLBCL and Hodgkin’s lymphoma (HL). We show that BLIMP1β expression is increased following the EBV infection of normal human tonsillar GC B cells. We also show that this change in expression is accompanied by hypomethylation of the BLIMP1β-specific promoter. Furthermore, we confirmed previous reports that the BLIMP1β promoter is hypomethylated in DLBCL cell lines and show for the first time that BLIMP1β is hypomethylated in the Hodgkin/Reed-Sternberg (HRS) cells of HL. Our results provide evidence in support of a role for BLIMP1β in the pathogenesis of EBV-associated B cell lymphomas.
|Publication status||Published - 8 Oct 2012|
- Epstein-Barr virus
- Hodgkin’s lymphoma
FingerprintDive into the research topics of 'Hypomethylation and over-expression of the beta isoform of BLIMP1 is Induced by Epstein-Barr virus infection of B Cells; potential implications for the pathogenesis of EBV-associated lymphomas'. Together they form a unique fingerprint.
- 1 Finished
The Contribution of Epstein-Barr Virus-Induced Epigenetic Changes to B Cell Differentiation and to the Pathogenesis of Hodgkin's Lymphoma
Murray, P., Rowe, M. & Woodman, C.
1/01/09 → 31/12/13