GPI Anchor-Deficient Erythrocytes Are Targeted for Destruction by Complement

When stem cells acquire a somatic mutation in the phosphatidylinositol glycan class A gene, they fail to synthesize GPI (glycosyl phosphatidylinositol),² which serves as an anchor for numerous membrane proteins. PNH blood cell clones have a total or partial deficiency in the GPI-anchored proteins CD 59 and CD 55, which are involved in complement regulation.^1,3 Blood cells show increased sensitivity to the lytic activity of complement.^1,3

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