Regulated expression of complement factor B in the human kidney.
We have previously demonstrated regulated expression of C3 in the proximal 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 examined factor B gene expression in human kidneys. 35S riboprobes were generated from a human factor B cDNA. By in situ hybridization, proximal tubular factor B message was seen in 17 kidneys with various nephropathies. The expression was most intense in organs with evidence of interstitial inflammation, and its localization paralleled the inflammation. As was the case with C3 and C4, there was never any evidence of glomerular factor B message, nor was any seen in infiltrating inflammatory cells. In eight normal kidney tissues, factor B expression was either absent or restricted to rare foci of interstitial infiltration. The proximal renal tubular epithelium of humans appears to express the genes for both components of the alternative pathway convertase, C3 and factor B. These locally produced components may be important mediators of the interstitial inflammation that is common to all progressive nephritides.
Welch
T R
TR
Division of Nephrology, Children's Hospital Research Foundation, Cincinnati, Ohio, USA.
Beischel
L S
LS
Frenzke
M
M
Witte
D
D
D001483:Base Sequence; D011415:Complement Factor B / Q000235:genetics*; D015342:DNA Probes / Q000235:genetics; D005786:Gene Expression Regulation; D005921:Glomerulonephritis / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007668:Kidney / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
D015342:DNA Probes; D012333:RNA, Messenger; D011415:Complement Factor B