First published April 1, 2014 - More info
Protection against deadly pathogens requires the production of high-affinity antibodies by B cells, which are generated in germinal centers (GCs). Alteration of the GC developmental program is common in many B cell malignancies. Identification of regulators of the GC response is crucial to develop targeted therapies for GC B cell dysfunctions, including lymphomas. The histone H3 lysine 27 methyltransferase enhancer of zeste homolog 2 (EZH2) is highly expressed in GC B cells and is often constitutively activated in GC-derived non-Hodgkin lymphomas (NHLs). The function of EZH2 in GC B cells remains largely unknown. Herein, we show that
Marieta Caganova, Chiara Carrisi, Gabriele Varano, Federica Mainoldi, Federica Zanardi, Pierre-Luc Germain, Laura George, Federica Alberghini, Luca Ferrarini, Asoke K. Talukder, Maurilio Ponzoni, Giuseppe Testa, Takuya Nojima, Claudio Doglioni, Daisuke Kitamura, Kai-M. Toellner, I-hsin Su, Stefano Casola
Original citation: J Clin Invest. 2013;123(12):5009–5022. doi:10.1172/JCI70626.
Citation for this corrigendum: J Clin Invest. 2014;124(4):1869. doi:10.1172/JCI75675.
During the preparation of the manuscript, the histogram plots for Figure 4F were inadvertently inverted. The correct figure panel is below.
The authors regret the error.