Macrophage colony-stimulating factor 1 receptor (CSF-1R) (CSF-1R)

Macrophage colony-stimulating factor 1 receptor (CSF-1R), also known as CD115 or c-Fms, is a type III receptor tyrosine kinase that plays a critical role in the development and maintenance of the mononuclear phagocyte system [1, 8]. It is primarily expressed on monocytes, macrophages, and osteoclasts, and is activated by its ligands, CSF-1 (M-CSF) and IL-34 [1, 5]. Upon ligand binding, the receptor undergoes dimerization and autophosphorylation, triggering downstream signaling pathways such as PI3K/Akt and MAPK that promote cell survival, proliferation, and differentiation [7, 9]. In many cancers, the CSF-1/CSF-1R axis is exploited to recruit tumor-associated macrophages (TAMs) that create an immunosuppressive environment and promote angiogenesis and metastasis [5, 13, 14]. Therapeutic targeting of CSF-1R, through small molecule inhibitors like pexidartinib or monoclonal antibodies like emactuzumab, aims to deplete these TAMs or reprogram them to an anti-tumor phenotype [2, 4, 5]. Beyond oncology, CSF-1R is a target of interest in neurodegenerative diseases like Alzheimer's due to its role in microglial regulation, and in inflammatory conditions such as rheumatoid arthritis [3, 8].

Other names

CSF1Rc-FmsCD115M-CSFRFMS proto-oncogeneMacrophage colony-stimulating factor receptorColony stimulating factor 1 receptor

Receptor tyrosine kinase inhibition, Ligand-binding inhibition, Inhibition of receptor dimerization