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Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2002-10-3068. This Article Full Text (PDF) All Versions of this Article: 2002-10-3068v1 101/12/5046    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yazdanbakhsh, K. Articles by Scaradavou, A. Search for Related Content PubMed PubMed Citation Articles by Yazdanbakhsh, K. Articles by Scaradavou, A. Social Bookmarking                   What's this? Submitted October 8, 2002 Accepted February 3, 2003 Complement Receptor 1 Inhibitors for Prevention of Immune-mediated Red Cell Destruction: Potential Use in Transfusion Therapy Karina Yazdanbakhsh*, Stanley Kang, Daniel Tamasauskas, Dorothy Sung, and Andromachi Scaradavou Complement Biology Research Program, New York Blood Center, New York, NY, USA National Cord Blood Program, New York Blood Center, New York, NY, USA * Corresponding author; email: karina_yazdanbakhsh{at}nybc.org. Activation of complement cascade via the antibody-mediated classical pathway can initiate red blood cell (RBC) destruction, causing transfusion reactions and hemolytic anemia. In the present study, we have assessed the ability of a human recombinant soluble form of complement receptor 1 (sCR1) to inhibit complement-mediated RBC destruction in vitro and in vivo. Using an in vitro alloimmune incompatibility model, sCR1 inhibited complement activation and prevented hemolysis. Following transfusion of human group O RBCs into mice lacking detectable pre-existing antibodies against the transfused RBCs, systemic co-administration of 10 mg/Kg of sCR1, a dose well tolerated in human subjects for prevention of tissue injury, completely inhibited the in vivo clearance of the transfused RBCs and surface C3 deposition in the first hour post-transfusion, correlating with the half-life of sCR1 in the circulation. Treatment with sCR1 increased the survival of transfused human group A RBCs in the circulation of mice with pre-existing anti-A for two hours post-transfusion by 50%, reduced intravascular hemolysis and lowered the levels of complement deposition (C3 and C4), but not IgG or IgM, on the transfused cells by 100 fold. We further identified potential functional domains in CR1 that can act to limit complement-mediated RBC destruction in vitro and in vivo. Collectively, our data highlight a potential use of CR1-based inhibitors for prevention of complement-dependent immune hemolysis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Mqadmi, X. Zheng, and K. Yazdanbakhsh CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia Blood, May 1, 2005; 105(9): 3746 - 3748. [Abstract] [Full Text] [PDF]

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