Csf2, also known as colony-stimulating factor 2 or granulocyte-macrophage colony-stimulating factor (GM-CSF), is a potent cytokine. It stimulates myeloid cells such as dendritic cells, macrophages, and microglia, and is involved in regulating inflammation, cell growth, and differentiation. The CSF2-STAT5 signaling pathway is among the associated pathways, and it plays an overall crucial role in various biological processes and disease conditions. Genetic models, especially KO/CKO mouse models, are valuable for studying its functions [2,4].

In the context of diseases, in antineutrophil cytoplasmic antibody-associated vasculitis (AAV), CCR2-/-chimeric mice (with reduced circulating classical monocytes) and CSF2rb-/-chimeric mice (lacking the CSF2 receptor subunit beta) were protected from necrotising crescentic glomerulonephritis (NCGN), indicating that Csf2-mediated monocyte activation is important in AAV pathogenesis [1]. In sepsis-induced acute kidney injury, administration of a Csf2-neutralizing antibody after cecal ligation and puncture (CLP) aggravated kidney injury, while recombinant mouse Csf2 protein rescued mice, suggesting Csf2 promotes alternative macrophage transition and protects against kidney injury [3]. In gliomas, CSF2-deficient human glioma cells transplanted to mouse brains failed to attract microglia, were smaller, and provided a survival benefit in tumour-bearing mice, showing that tumour-derived Csf2 controls myeloid cell accumulation and glioma progression [5].

In conclusion, Csf2 is essential in regulating inflammation and cell-specific functions in myeloid cells. Model-based research, especially using KO/CKO mouse models, has revealed its significant roles in diseases such as AAV, sepsis-induced acute kidney injury, and gliomas. Understanding Csf2 functions can potentially lead to new therapeutic strategies for these diseases.