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An extended mini-complement factor H molecule ameliorates experimental C3 glomerulopathy #MMPMID26221753
Kidney Int 2015[Dec]; 88 (6): 1314-22 PMID26221753show ga
Abnormal regulation of the complement alternative pathway is associated with C3 glomerulopathy. Complement factor H is the main plasma regulator of the alternative pathway and consists of 20 short consensus repeat (SCR) domains. Although recombinant full-length factor H represents a logical treatment for C3 glomerulopathy, its production has proved challenging. We and others have designed recombinant mini-factor H proteins in which ?non-essential' SCR domains have been removed. Here, we report the in vitro and in vivo effects of a mini-complement factor H protein, FH1?5^18?20, using the unique factor H?deficient (Cfh?/?) mouse model of C3 glomerulopathy. FH1?5^18?20 is comprised of the key complement regulatory domains (SCRs 1?5) linked to the surface recognition domains (SCRs 18?20). Intraperitoneal injection of FH1?5^18?20 in Cfh?/? mice reduced abnormal glomerular C3 deposition, similar to full-length factor H. Systemic effects on plasma alternative pathway control were comparatively modest, in association with a short half-life. Thus, FH1?5^18?20 is a potential therapeutic agent for C3 glomerulopathy and other renal conditions with alternative pathway-mediated tissue injury.