Stepwise reprogramming of B cells into macrophages

Huafeng Xie, Min Ye, Ru Feng, Thomas Graf



Starting with multipotent progenitors, hematopoietic lineages are specified by lineage-restricted transcription factors. The transcription factors that determine the decision between lymphoid and myeloid cell fates, and the underlying mechanisms, remain largely unknown. Here, we report that enforced expression of C/EBPα and C/EBPβ in differentiated B cells leads to their rapid and efficient reprogramming into macrophages. C/EBPs induce these changes by inhibiting the B cell commitment transcription factor Pax5, leading to the downregulation of its target CD19, and synergizing with endogenous PU.1, an ETS family factor, leading to the upregulation of its target Mac-1 and other myeloid markers. The two processes can be uncoupled, since, in PU.1-deficient pre-B cells, C/EBPs induce CD19 downregulation but not Mac-1 activation. Our observations indicate that C/EBPα and β remodel the transcription network of B cells into that of macrophages through a series of parallel and sequential changes that require endogenous PU.1. Cell 2004

bits of bio by Thomas Moreau

Thomas Moreau, Head of Research at, presenting the first of two seminal papers (both on reprogramming in blood cells): Stepwise reprogramming of B cells into macrophages (Huafeng Xie, Min Ye, Ru Feng, Thomas Graf)


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