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Structural and functional differences between decay-accelerating factor and red cell acetylcholinesterase.

J Sugarman, D V Devine, W F Rosse

    Blood
    |September 1, 1986
    PubMed
    Summary
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    Paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes lack acetylcholinesterase (AChE) and decay-accelerating factor (DAF) activities. Studies confirm AChE and DAF are distinct proteins, both absent in PNH cells.

    Area of Science:

    • Hematology
    • Immunology
    • Biochemistry

    Background:

    • Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by abnormal erythrocytes lacking specific protein activities.
    • Acetylcholinesterase (AChE) and decay-accelerating factor (DAF) are glycoproteins found on normal erythrocytes, but their distinctness in PNH has been questioned.

    Purpose of the Study:

    • To determine if acetylcholinesterase (AChE) and decay-accelerating factor (DAF) activities reside on separate proteins in erythrocytes.
    • To confirm the absence of both AChE and DAF on PNH erythrocytes.

    Main Methods:

    • Utilized antibody binding assays to assess cross-inhibition between AChE and DAF.
    • Investigated the effect of inhibiting DAF and AChE activity on erythrocyte susceptibility to complement-mediated lysis.

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  • Examined the role of DAF and AChE in regulating the classical complement pathway's C3 convertase complex.
  • Employed immunoprecipitation to isolate and identify AChE and DAF.

    • Main Results:

    • Antibody binding to DAF did not inhibit AChE binding or activity, and vice versa, indicating distinct proteins.
    • Inhibition of DAF, but not AChE, increased erythrocyte sensitivity to complement lysis.
    • DAF, but not AChE, inhibited the decay of the C3 convertase complex.
    • Immunoprecipitation confirmed that AChE and DAF could be isolated independently.

    Conclusions:

    • Acetylcholinesterase (AChE) and decay-accelerating factor (DAF) are indeed separate proteins.
    • Both PNH II and PNH III erythrocytes lack both distinct AChE and DAF proteins.