CSF1 biology

Circulating CSF-1 is believed to be derived from endothelial cells lining the small blood vessels. Ninety-four per cent of circulating CSE-I (half-life lOmin) is cleared by CSF-lR-mediated endocytosis and intracellular degradation by Kupffer cells of the liver and splenic macrophages, only 5% being filtered through the kidney. This clearance mechanism represents a coarse negative feedback control on macrophage production, whereby the number of sinusoidally located end cells determines the steady-state concentration of circulating growth factor. In addition, CSF-1 is synthesized locally by osteoblasts and epithelial cells of the female reproductive tract. By virtue of local synthesis of the long-lived cell surface CSF-1 and of localized sequestration of the secreted proteoglycan CSF-1, both these forms may participate in short-range regulation of target cells (Figure 1).

The mouse mutation, osteopetrotic (op), is an inactivating mutation in the CSF-1 gene. While many of the overt phenotypes of the op/op mouse (Table 1) are significantly corrected by restoration of circulating CSF-1, failure to qualitatively rescue several phenotypes by daily injection with human recombinant CSF-1 (e.g. Table 2), indicates that CSF-1 also acts locally. Studies in op/op mice have established the central role of CSF-1 in the regulation of cell surface

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