Figure 5
Figure 5. PR3 neutrophil membrane display depends on GPI linkers. Neutrophils subjected to GPI-anchor cleavage by phospholipase C showed decreased membrane NB1 and PR3 expression (A, dotted lines) as compared with control cells (bold lines). The mean change of fluorescence in 7 independent experiments was −43% ± 4% for NB1 and −33% ± 12% for PR3, P < .05. Error bars indicate SEM; *P < .05; **P < .01. (B). The β2-integrin CD18, a marker of cell activation, remained unchanged (6 ± 6). (C) NB1 and several other GPI-linked proteins are expressed on neutrophils from a patient with PNH in comparison to a healthy control subject. Isotype control antibody staining is shown by the thin line and the GPI-linked molecule staining by bold lines. PNH is characterized by an acquired deficiency in GPI-linker synthesis. Membrane display of GPI-linked proteins was strongly decreased, with mNB1 and mPR3 expression even being absent in the patient was PNH.

PR3 neutrophil membrane display depends on GPI linkers. Neutrophils subjected to GPI-anchor cleavage by phospholipase C showed decreased membrane NB1 and PR3 expression (A, dotted lines) as compared with control cells (bold lines). The mean change of fluorescence in 7 independent experiments was −43% ± 4% for NB1 and −33% ± 12% for PR3, P < .05. Error bars indicate SEM; *P < .05; **P < .01. (B). The β2-integrin CD18, a marker of cell activation, remained unchanged (6 ± 6). (C) NB1 and several other GPI-linked proteins are expressed on neutrophils from a patient with PNH in comparison to a healthy control subject. Isotype control antibody staining is shown by the thin line and the GPI-linked molecule staining by bold lines. PNH is characterized by an acquired deficiency in GPI-linker synthesis. Membrane display of GPI-linked proteins was strongly decreased, with mNB1 and mPR3 expression even being absent in the patient was PNH.

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