Abstract
The human erythrocyte transmembrane sialoglycoprotein, glycophorin C (GYPC), plays a functional role in regulating red cell shape and mechanical stability. Antibodies to GYPC cause hemolytic disease of the fetus and newborn (HDFN) that is associated with classical Fcγ receptor-mediated phagocytosis. However, in vitro clonogenic studies with cord blood progenitor cells suggest that anti-GYPC also suppresses erythropoiesis, which is consistent with the observations of severe and early fetal anemia and late onset neonatal anemia [
Transfus Med
2005
;15
:125
–32Brit J Haematol
2006
;133
:443
–4Mitochondrial Membrane Potential Disruption by Anti-GYPC
Author notes
Disclosure: No relevant conflicts of interest to declare.
2007, The American Society of Hematology
2007
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