Binding of factor H to tubular epithelial cells limits interstitial complement activation in ischemic injury.

ABSTRACT: Factor H is a regulator of the alternative pathway of complement, and genetic studies have shown that patients with mutations in factor H are at increased risk for several types of renal disease. Pathogenic activation of the alternative pathway in acquired diseases, such as ischemic acute kidney injury, suggests that native factor H has a limited capacity to control the alternative pathway in the kidney. Here we found that an absolute deficiency of factor H produced by gene deletion prevented complement activation on tubulointerstitial cells after ischemia/reperfusion (I/R) injury, likely because alternative pathway proteins were consumed in the fluid phase. In contrast, when fluid-phase regulation by factor H was maintained while the interaction of factor H with cell surfaces was blocked

SUBMITTER: Renner B 

PROVIDER: S-EPMC3133686 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature