Figure 5
Figure 5. GM-CSF–induced regulation of the DC transcriptional program mediated through STAT5 and canonical NF-κB. STAT5 and canonical NF-κB transcription factors can directly regulate the DC transcriptional program. Regulation of RelB, IRF4, and PU.1 expression not only promotes DC differentiation in general but may also influence subset distribution among the DCs generated. The role of C/EBPα is also subset-specific, promoting development of interstitial DCs through potentiating the commitment of multipotent hematopoietic progenitors to the granulocyte/macrophage lineage, but inhibiting Langerhans cell development. The inhibitory actions of STAT5 toward IRF8 and SpiB explain the negative impact GM-CSF has on the plasmacytoid DC lineage, whereas effects on genes involved in DC functionality may promote the immunogenicity of DC differentiated with GM-CSF.

GM-CSF–induced regulation of the DC transcriptional program mediated through STAT5 and canonical NF-κB. STAT5 and canonical NF-κB transcription factors can directly regulate the DC transcriptional program. Regulation of RelB, IRF4, and PU.1 expression not only promotes DC differentiation in general but may also influence subset distribution among the DCs generated. The role of C/EBPα is also subset-specific, promoting development of interstitial DCs through potentiating the commitment of multipotent hematopoietic progenitors to the granulocyte/macrophage lineage, but inhibiting Langerhans cell development. The inhibitory actions of STAT5 toward IRF8 and SpiB explain the negative impact GM-CSF has on the plasmacytoid DC lineage, whereas effects on genes involved in DC functionality may promote the immunogenicity of DC differentiated with GM-CSF.

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