Journal
IMMUNITY
Volume 18, Issue 2, Pages 217-227Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(03)00022-0
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- NIDDK NIH HHS [DK062994, DK52855, DK60979] Funding Source: Medline
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Basal complement activity presents a potential danger for self cells that are tightly protected by complement regulators including CD59. Mice express two Cd59 genes (mCd59a and mCd59b); mCd59b has approximately a 6-fold higher specific activity than mCd59a. Consistently, mCd59b knockout mice present a strong phenotype characterized by hemolytic anemia with increased reticulocytes, anisopoikilocytosis, echinocytosis, schistocytosis, free hemoglobin in plasma, hemoglobinuria with hemosiderinuria and platelet activation. Remarkably, mCd59b(-/-) males express a progressive loss of fertility associated with immobile dysmorphic and fewer sperm cells after 5 months of age. This work indicates that mCd59b is a key complement regulator in mice and that CD59 is critical in protecting self cells; it also provides a novel model to study complement regulation in human diseases.
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