Csf3, also known as colony-stimulating factor 3 or G-CSF, is a key cytokine in neutrophil production and function. It stimulates the maturation, proliferation, and trafficking of myeloid progenitor cells, and is involved in cytokine-cytokine receptor interaction pathways [1,3]. Its biological importance lies in its role in maintaining normal neutrophil levels and immune responses. Genetic models, such as gene knockout mouse models, have been crucial in understanding its functions.

In humans, biallelic inactivating variants in Csf3 have been found to cause a novel autosomal recessive form of severe congenital neutropenia (SCN), mirroring the phenotype observed in mouse and zebrafish models of Csf3 deficiency [1]. In mouse models of acute exacerbation of pulmonary fibrosis (AE-PF), exogenous Csf3 protein exacerbates the condition by disrupting alveolar epithelial barrier integrity via the PI3K/p-Akt/Snail pathway [2].

In conclusion, Csf3 is essential for neutrophil-related biological functions. The study of Csf3 knockout mouse models has revealed its significant role in diseases like SCN and AE-PF, enhancing our understanding of the underlying mechanisms and potentially guiding future therapeutic strategies for these conditions.