Colony Stimulating Factor-1 (CSF-1) is the primary regulator of the survival, proliferation and differentiation of mononuclear phagocytes. All of the effects of CSF-1 are mediated by the high affinity CSF-1 receptor (CSF-1R), a protein tyrosine kinase encoded by the c-fms proto-oncogene. Previous studies have shown that the phenotype of CSF-1 receptor-deficient (Csf1r−/−) mice is more severe than the phenotype of CSF-1-deficient (Csf1op/op) mice. Csf1r−/− mice have a more severe osteopetrosis, fewer osteoclasts, lower survival and fewer tissue macrophages and these differences are more pronounced on single strain backgrounds. This led us to speculate that there may be another ligand for the CSF-1R (
Disclosures: No relevant conflicts of interest to declare.
[Supported in part by NIH grant CA 32551 (ERS)].