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Abstract
The amounts of colony-stimulating factor (CSF-1) produced by the mesangial cells of the kidney may be of pivotal importance in determining the outcome of nephritis, since CSF-1 activates macrophages, and macrophages have been shown to perform an important scavenger function in removing immune complexes which localize in the kidney. To test this hypothesis, the present study examined CSF-1 production by mesangial cells of the autoimmune MRL/MpJ-Ipr-Ipr strain of mice and also of their normal congenic MRL/MpJ -++ counterparts. It was found that mesangial cells of autoimmune mice produced diminished amounts of functional CSF-1 when measured by a bioassay, giving validation to the hypothesis proposed. Of interest, expression of CSF-1 mRNA was discordantly increased in mesangial cells of the MRL-Ipr autoimmune mice. Based on current knowledge of the pathway for CSF-1 synthesis and secretion, it would appear that there may be a block in the post-transcriptional pathway for CSF-1 biosynthesis in autoimmune mesangial cells.