The Journal of Experimental Medicine
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Published online 18 December 2000.
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© The Rockefeller University Press, 0022-1007/2000/12/1841/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 12, December 18, 2000 1841-1848

Brief Definitive Report

Suppression of Signal Transducer and Activator of Transcription 3–Dependent B Lymphocyte Terminal Differentiation by Bcl-6

Rajko Reljica, Simon D. Wagnera,b, Luke J. Peakmana, and Douglas T. Fearona

a Wellcome Trust Immunology Unit, University of Cambridge, School of Clinical Medicine, Cambridge CB2 2SP, United Kingdom
b Department of Haematology, Addenbrookes Hospital, Cambridge CB2 2SP, United Kingdom
Wellcome Trust Immunology Unit, MRC Centre, Hills Road, Cambridge CB2 2SP, UK.44-1223-33681744-1223-330528

dtf1000{at}cus.cam.ac.uk

Lymphocytes usually differentiate into effector cells within days after antigen exposure, except in germinal centers where terminal differentiation is delayed while somatic hypermutation creates high-affinity antibody mutants. Here we investigate whether arrest of terminal differentiation can be mediated by BCL-6, a transcriptional repressor that is expressed by germinal center B cells and is required for this phase of B cell development. We find that BCL-6 suppresses the differentiation of transformed and primary B cells to plasma cells by inhibiting the signal transducer and activator of transcription 3–dependent expression of the major regulator of plasma cell development, the B lymphocyte–induced maturation protein (Blimp-1). This function of BCL-6 as a repressor of B lymphocyte differentiation may also underlie the association between chromosomal translocations of its gene and B cell lymphomas.

Key Words: BTB-POZ protein • plasma cell • germinal center • retrovirus • interleukins

R. Reljic and S.D. Wagner contributed equally to this work.

© 2000 The Rockefeller University Press


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