Abstract:
:Recent demonstration that Cromer-related human blood group antigens reside on decay-accelerating factor (DAF) has led to identification of an apparent null phenotype (Inab) for erythrocyte DAF. This study examined expression of other phosphatidylinositol (PI)-anchored proteins by Inab erythrocytes and showed that the PI-linked membrane proteins acetylcholinesterase (AchE) and lymphocyte function-associated antigen-3 (LFA-3) are normally expressed by these cells. Furthermore, studies of the complement sensitivity of Inab RBCs demonstrated them to be abnormally complement sensitive, with an apparent defect in downregulation of C3 convertase activity. Thus, the Inab phenotype appears to represent an instance of hereditary erythrocyte DAF deficiency whose mechanism differs from that of paroxysmal nocturnal hemoglobinuria (PNH) and which is unassociated with clinically evident hemolytic disease.
journal_name
Bloodjournal_title
Bloodauthors
Telen MJ,Green AMsubject
Has Abstractpub_date
1989-07-01 00:00:00pages
437-41issue
1eissn
0006-4971issn
1528-0020journal_volume
74pub_type
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