Controlling the complement system for prevention of red cell destruction.
OBJECTIVE
Complement sensitization of red blood cells (RBCs) can lead to both intravascular and extravascular red cell destruction. Altered levels of naturally occurring complement regulatory proteins on red cells can result in hemolysis, while defective expression of these proteins on immune cells can cause breakdown of tolerance to self antigens and is associated with autoimmune disease.


RESULTS
To date several complement inhibitors, including recombinant forms of complement regulatory proteins, humanized antibodies, and synthetic molecules have been described that limit complement activation by interfering with different steps in the complement cascade. However, few have been evaluated for prevention of complement-mediated RBC destruction. In this review, possible applications of these complement inhibitors for treatment of complement-mediated hemolysis in specific disease states are described. Furthermore, the implication of the regulatory role of complement in the development of autoimmune hemolytic anemia is discussed.


CONCLUSIONS
Complement therapeutics has potential for effective and safe prophylactic use and treatment of hemolytic transfusion reactions and complement-mediated hemolytic diseases. Furthermore, the regulatory function of complement may be exploited to prevent and treat autoimmune hemolytic anemia.
Yazdanbakhsh
Karina
K
Complement Biology, New York Blood Center, New York, NY 10021, USA. kyazdanbakhsh@nybloodcenter.org
D000743:Anemia, Hemolytic / Q000188:drug therapy / Q000517:prevention & control; D003169:Complement Inactivator Proteins / Q000494:pharmacology* / Q000627:therapeutic use; D003165:Complement System Proteins / Q000502:physiology*; D006461:Hemolysis / Q000187:drug effects*; D006801:Humans
D003169:Complement Inactivator Proteins; D003165:Complement System Proteins