Deficiency of DAF and Crry on murine platelets leads to complement-dependent clearance via the macrophage phagocytic receptor CRIg
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چکیده
Address correspondence and reprint requests to: Dr. Wen-Chao Song Institute for Translational Medicine and Therapeutics and Department of Pharmacology University of Pennsylvania School of Medicine, Rm 1254 BRBII/III, 421 Curie Blvd Philadelphia, PA 19104, Tel: 215-573-6641, Fax: 215-746-8941 [email protected] Blood First Edition Paper, prepublished online June 4, 2008; DOI 10.1182/blood-2008-01-134304
منابع مشابه
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.
Complement activation on human platelets is known to cause platelet degranulation and activation. To evaluate how normal platelets escape complement attack in vivo, we studied the fate of murine platelets deficient in 2 membrane complement regulatory proteins using an adoptive transfer model. We show here that deficiency of either decay-accelerating factor (DAF) or complement receptor 1-related...
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Decay-accelerating factor (DAF) and complement receptor 1-related gene/protein y (Crry) are two membrane-bound complement regulators on murine erythrocytes that inhibit C3/C5 convertases. Previously, we found that Crry- but not DAF-deficient erythrocytes were susceptible to alternative pathway complement-mediated elimination in vivo. To determine whether it is a unique activity or a higher leve...
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Decay-accelerating factor (DAF) and complement receptor 1-related gene/protein y (Crry) are two membrane-anchored complement regulatory proteins in rodent. Although both proteins are broadly distributed and exert complement regulation at the same steps of the complement cascade, DAF knockout mice are viable whereas Crry knockout mice die in utero as a result of maternal complement attack. The l...
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The role of complement in the pathogenesis of autoimmune hemolytic anemia (AIHA) has been controversial and may depend on a number of factors, including the affinity and isotype of the pathogenic antibodies involved. We have recently shown that mouse erythrocytes deficient in the membrane C3 regulatory protein, complement receptor 1–related gene/ protein y (Crry), but not decay-accelerating fac...
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تاریخ انتشار 2008