LOCALIZATION OF THE COMPLEMENT REGULATORY PROTEINS IN THE NORMAL HUMAN KIDNEY

Citation
S. Ichida et al., LOCALIZATION OF THE COMPLEMENT REGULATORY PROTEINS IN THE NORMAL HUMAN KIDNEY, Kidney international, 46(1), 1994, pp. 89-96
Citations number
42
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
46
Issue
1
Year of publication
1994
Pages
89 - 96
Database
ISI
SICI code
0085-2538(1994)46:1<89:LOTCRP>2.0.ZU;2-#
Abstract
The kidney is an organ where complement-mediated tissue injuries take place by various stimuli. To assess how the kidney is protected from t he autologous complement attack, comparative localization of decay acc elerating factor (DAF), membrane cofactor protein (MCP) and 20 kDa hom ologous restriction factor (HRF20) was studied in the normal human kid ney. Specific monoclonal antibodies to DAF, MCP and HRF20 were used fo r the study. Studies by immunofluorescence and immunoelectron microsco py showed that the distribution of each protein in the kidney was comp lementary to each other in most parts. MCP and HRF20 were clearly seen in the glomerular capillaries, while DAF was only faintly observed. J uxtaglomerular apparatus was abundant in DAF and MCP but not in HRF20. HRF20 was most strongly expressed in the peritubular capillaries wher e MCP was not detectable. Basolateral membranes of the proximal tubule s and collecting ducts expressed MCP strongly, while there was no expr ession of DAF in the proximal tubules. Interestingly, both DAF and MCP , which inhibit complement activation at C3/C4 level, were not express ed in the apical portion of the tubular cells including proximal tubul e brush border. In contrast, HRF20 was expressed on the apical part of the tubules. Medullary interstitium strongly expressed MCP but not DA F. Based on these observations, we conclude that each segment of the k idney is protected from the complement attack by the different combina tion of complement regulatory proteins. We speculate that the tubular cells might be fragile when complements are activated inside the tubul ar lumen, because there is no expression of complement regulatory prot eins which inhibit C3 convertase.