| First Author | Qin X | Year | 2003 |
| Journal | Immunity | Volume | 18 |
| Issue | 2 | Pages | 217-27 |
| PubMed ID | 12594949 | Mgi Jnum | J:82330 |
| Mgi Id | MGI:2652297 | Doi | 10.1016/s1074-7613(03)00022-0 |
| Citation | Qin X, et al. (2003) Deficiency of the mouse complement regulatory protein mCd59b results in spontaneous hemolytic anemia with platelet activation and progressive male infertility. Immunity 18(2):217-27 |
| abstractText | 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. |
