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 Blood, 15 September 2007, Vol. 110, No. 6, pp. 2190-2192.
Prepublished online as a Blood First Edition Paper on June 6, 2007; DOI 10.1182/blood-2007-04-083170.

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RED CELLS

Brief Report

Factor H–mediated cell surface protection from complement is critical for the survival of PNH erythrocytes

Viviana P. Ferreira1, and Michael K. Pangburn1

1 Department of Biochemistry, Center for Biomedical Research, University of Texas Health Science Center, Tyler

Paroxysmal nocturnal hemoglobinuria (PNH) cells are partially (type II) or completely (type III) deficient in GPI-linked complement regulatory proteins CD59 and CD55. PNH III erythrocytes circulate 6 to 60 days in vivo. Why these cells are not lysed as rapidly by complement as unprotected foreign cells, which normally lyse within minutes, remains undetermined. Factor H plays a key role in the homeostasis of complement in fluid phase and on cell surfaces. We have recently shown that a recombinant protein encompassing the C-terminus of factor H (rH19-20) specifically blocks cell-surface complement regulatory functions of factor H without affecting fluid-phase control of complement. Here we show that PNH II and III cells become highly susceptible to complement-mediated lysis by nonacidified normal human serum in vitro, when the cell surface complement-regulatory functions of factor H are blocked. The results indicate that cells deficient in surface-bound regulators are protected for extended periods of time by factor H.


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D. D. Kim, T. Miwa, Y. Kimura, R. A. Schwendener, M. van Lookeren Campagne, and W.-C. Song
Deficiency of decay-accelerating factor and complement receptor 1-related gene/protein y on murine platelets leads to complement-dependent clearance by the macrophage phagocytic receptor CRIg
Blood, August 15, 2008; 112(4): 1109 - 1119.
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