REGULATED EXPRESSION OF COMPLEMENT FACTOR-B IN THE HUMAN KIDNEY

We have previously demonstrated regulated expression of C3 in the prox imal renal tubular epithelial cells of humans. To test the hypothesis that local alternative pathway complement activation could contribute to the tubulointerstitial component of chronic renal disease, we exami ned factor B gene expression in human kidneys. S-35 riboprobes were ge nerated from a human factor B cDNA. By in situ hybridization, proximal tubular factor B message was seen in 17 kidneys with various nephropa thies. The expression was most intense in organs with evidence of inte rstitial inflammation, and its localization paralleled the inflammatio n. As was the case with C3 and C4, there was never any evidence of glo merular factor B message, not was any seen in infiltrating inflammator y cells. In eight normal kidney tissues, factor B expression was eithe r absent or restricted to rare foci of interstitial infiltration. The proximal renal tubular epithelium of humans appears to express the gen es for both components of the alternative pathway convertase, C3 and f actor B. These locally produced components may be important mediators of the interstitial inflammation that is common to all progressive nep hritides.