pERKing up the BLIMP in plasma cell differentiation

University of Pennsylvania School of Medicine, John Morgan Building, 3620 Hamilton Walk, Philadelphia, PA 19104, USA.
Science Signaling (Impact Factor: 6.28). 04/2011; 4(169):pe21. DOI: 10.1126/scisignal.2001987
Source: PubMed


The intracellular pathways that induce the differentiation of naïve B cells into antibody-secreting plasma cells remain poorly defined. A new study now provides surprising evidence that the activation of extracellular signal-regulated kinase (ERK) is pivotal for inducing the transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp-1), which is required for plasma cell differentiation. Consequently, ERK-deficient B cells were unable to generate plasma cells effectively. This is an unexpected result, because previous work has shown that ERK signaling functions chiefly to induce cell division, whereas plasma cells are considered to be nondividing, terminally differentiated cells. This finding not only reveals an important signaling pathway that underlies antibody-mediated immunity but also raises important questions about the varying roles that ERK, and perhaps other kinases, may play in different biological contexts.

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    • "Control of terminal B cell differentiation by transcription factors operates following specific timing and pace that remain only partially understood. A large number of external and internal signals and cues impact this process by influencing transcriptional cascades (Allman and Cancro, 2011). BCL6 has an antagonistic role to the plasmablast fate-determining transcription factor BLIMP1, encoded by PRDM1, in lineage determination. "
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