Common mechanisms for the regulation of B cell differentiation and transformation by the transcriptional repressor protein BCL-6

Saritha Kusam, Alexander Dent

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The BCL-6 transcriptional repressor protein is a critical regulator of normal B cell differentiation and BCL-6 has recently been shown to act as an oncogene in several mouse model systems. The molecular pathways by which BCL-6 regulates B cell differentiation and also promotes the transformation of primary B cells are undoubtedly related; however, these pathways are poorly understood. The commonly accepted model for BCL-6 function in B cells is that BCL-6 inhibits the terminal differentiation of activated B cells into plasma cells and that deregulation of BCL-6 expression leads to an inhibition of terminal differentiation and continued proliferation. BCL-6 induces a germinal-center phenotype in primary B cells by unknown mechanisms, and can reverse the terminal differentiation of plasma cell tumor lines. BCL-6 can promote the immortalization of primary B cells and can augment telomerase activity. The role of the vast majority of BCL-6 target genes and interacting proteins in normal B cell differentiation and B cell transformation is essentially unresolved and is an important area for future investigation.

Original languageEnglish
Pages (from-to)177-186
Number of pages10
JournalImmunologic Research
Volume37
Issue number3
DOIs
StatePublished - Mar 2007

Fingerprint

Repressor Proteins
Cell Differentiation
B-Lymphocytes
Germinal Center
Plasmacytoma
Telomerase
Plasma Cells
Oncogenes
Phenotype
Cell Line

Keywords

  • B cell
  • BCL-6
  • bcl6
  • Differentiation
  • Germinal center
  • Immortalization
  • Non-Hodgkin's lymphoma
  • Plasma cell
  • Telomerase

ASJC Scopus subject areas

  • Immunology

Cite this

Common mechanisms for the regulation of B cell differentiation and transformation by the transcriptional repressor protein BCL-6. / Kusam, Saritha; Dent, Alexander.

In: Immunologic Research, Vol. 37, No. 3, 03.2007, p. 177-186.

Research output: Contribution to journalArticle

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