Control of inflammation, cytokine expression, and germinal center formation by BCL-6

Alexander L. Dent, Arthur L. Shaffer, Xin Yu, David Allman, Louis M. Staudt

Research output: Contribution to journalArticle

710 Scopus citations

Abstract

The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted BCL-6 gene developed myocarditis and pulmonary vasculitis, had no germinal centers, and had increased expression of T helper cell type 2 cytokines. The BCL-6 DNA recognition motif resembled sites bound by the STAT (signal transducers and activators of transcription) transcription factors, which mediate cytokine signaling. BCL-6 could repress interleukin-4 (IL-4)- induced transcription when bound to a site recognized by the IL-4-responsive transcription factor Stat6. Thus, dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6 -deficient mice and participate in lymphoid malignancies.

Original languageEnglish (US)
Pages (from-to)589-592
Number of pages4
JournalScience
Volume276
Issue number5312
DOIs
StatePublished - Apr 25 1997

    Fingerprint

ASJC Scopus subject areas

  • General

Cite this