| Summary: | <p>Abstract</p> <p>Background</p> <p>The B cell antigen receptor (BCR) is a signaling complex that mediates the differentiation of stage-specific cell fate decisions in B lymphocytes. While several studies have shown differences in signal transduction components as being key to contrasting phenotypic outcomes, little is known about the differential BCR-triggered gene transcription downstream of the signaling cascades.</p> <p>Results</p> <p>Here we define the transcriptional changes that underlie BCR-induced apoptosis and proliferation of immature and mature B cells, respectively. Comparative genome-wide expression profiling identified 24 genes that discriminated between the early responses of the two cell types to BCR stimulation. Using mice with a conditional <it>Myc</it>-deletion, we validated the microarray data by demonstrating that <it>Myc </it>is critical to promoting BCR-triggered B-cell proliferation. We further investigated the <it>Myc-</it>dependent molecular mechanisms and found that <it>Myc </it>promotes a BCR-dependent clonal expansion of mature B cells by inducing proliferation and inhibiting differentiation.</p> <p>Conclusion</p> <p>This work provides the first comprehensive analysis of the early transcriptional events that lead to either deletion or clonal expansion of B cells upon antigen recognition, and demonstrates that <it>Myc </it>functions as the hub of a transcriptional network that control B-cell fate in the periphery.</p>
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