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 and macrophages, and is involved in many biological processes including inflammation regulation and cell growth [3]. CSF2 is associated with multiple pathways such as the Akt/Mtor, p-Stat5, and Notch pathways, and plays a role in various diseases [2,4,5]. Genetic models, especially KO/CKO mouse models, are valuable for studying its functions.

In ANCA-induced glomerulonephritis, CCR2 -/- chimeric mice (lacking classical monocytes) and CSF2rb -/- chimeric mice (deficient in CSF2 receptor subunit beta) were protected from necrotizing crescentic glomerulonephritis, indicating that CSF2-dependent monocyte activation is crucial for the disease [1]. In sepsis-induced acute kidney injury, intraperitoneal injection of a Csf2-neutralizing antibody after cecal ligation and puncture aggravated kidney injury, while recombinant mouse Csf2 protein rescued mice, suggesting Csf2 promotes alternative macrophage transition and is beneficial for kidney repair [4]. In gliomas, knockdown of CSF2 in glioma cells reduced microglia-dependent glioma invasion, and CSF2-depleted gliomas were smaller with less microglia and macrophage infiltration, showing that tumour-derived CSF2 controls myeloid cell accumulation and glioma progression [6].

In summary, Csf2 is essential in regulating inflammation, macrophage transition, and cancer-related processes. Studies using KO/CKO mouse models have revealed its roles in diseases like ANCA-induced glomerulonephritis, sepsis-induced acute kidney injury, and gliomas. Understanding Csf2's functions through these models provides insights into disease mechanisms and potential therapeutic targets.