MafB, a transcription factor, is crucial in regulating macrophage differentiation. It is involved in various macrophage-related biological processes and associated with multiple diseases. Macrophage-specific gene knockout mouse models are valuable for studying its functions in vivo [1,2].

Using macrophage-specific Mafb-deficient (Mafbf/f::LysM-Cre) mice, studies have shown that Mafb deficiency in macrophages reduces thermogenesis, energy expenditure, and sympathetic neuron density in brown adipose tissue under cold conditions. This phenotype is characterized by a pro-inflammatory environment, macrophage/granulocyte accumulation, increased interleukin-6 production, and reduced nerve growth factor expression [2]. Also, myeloid MafB-deficient mice demonstrate increased systemic and lung IL-1β production in response to LPS treatment and Pseudomonas aeruginosa infection, indicating MafB as an important negative regulator of the NLRP3 inflammasome [3].

In conclusion, MafB is essential for regulating macrophages, maintaining systemic homeostasis, and is involved in diseases such as atherosclerosis, autoimmunity, obesity, ischemic stroke, and cold-induced BAT thermogenesis-related disorders. The use of MafB-deficient mouse models has provided insights into its role in these disease-related biological processes, highlighting its potential as a therapeutic target for macrophage-related diseases [1,2].