Transcriptome analysis of wild type and MafB knockout macrophages stimulated for 24 h with IL-4

Identifying a key regulator to control macrophage polarization is of great importance in the therapeutic strategies for modulating macrophage function to improve clinical outcome. Here, we identify MafB as an essential transcription factor to induce M2 macrophage polarization.

The myeloid-specific genetic ablation of Mafb in mice causes a severe defect in M2 macrophage polarization, ultimately leading to a deterioration of inflammatory diseases such as experimental sepsis or colitis.