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Additional forms of human decay-accelerating factor (DAF).

T Seya, T Farries, M Nickells

    Journal of Immunology (Baltimore, Md. : 1950)
    |August 15, 1987
    PubMed
    Summary
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    Decay-accelerating factor (DAF) fragments, DAF-A and DAF-B, retain fluid-phase complement inhibition but lose cell-bound activity. Endogenous enzymes likely cleave DAF, altering its membrane anchor.

    Area of Science:

    • Biochemistry
    • Immunology
    • Complement System

    Background:

    • Decay-accelerating factor (DAF) is a 65,000 Mr glycoprotein on human erythrocytes, crucial for regulating complement activation via a glycolipid anchor.
    • During DAF purification, two lower molecular weight forms, DAF-A (63,000 Mr) and DAF-B (55,000 Mr), were identified.

    Purpose of the Study:

    • To characterize the biochemical properties and functional activities of DAF-A and DAF-B.
    • To investigate the potential cleavage of DAF by endogenous enzymes on erythrocyte membranes.

    Main Methods:

    • Fluid-phase and cell-bound complement convertase decay assays were used to assess DAF fragment activity.
    • Molecular sieve high-pressure liquid chromatography (HPLC) analyzed the aggregation state and molecular weight of DAF forms.

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  • Surface-labeled erythrocytes were treated with phosphatidyl inositol-specific phospholipase C, papain, or leukocytes to identify DAF cleavage products.

    • Main Results:

    • Both DAF-A and DAF-B inhibited fluid-phase C3 convertases but failed to inhibit cell-bound convertases, indicating altered membrane anchoring.
    • DAF-A existed in an aggregated form (approx. 450,000 Mr) and bound to hydrophobic columns, while DAF-B eluted as a monomer (approx. 60,000 Mr).
    • Papain efficiently released a DAF-B-sized fragment, and leukocyte incubation mimicked papain digestion, suggesting protease involvement in DAF cleavage.

    Conclusions:

    • DAF fragments generated by enzymatic cleavage lose their ability to associate with cell membranes, impairing their function in regulating cell-bound complement.
    • Endogenous phospholipases and proteases are hypothesized to cleave DAF, producing fragments analogous to DAF-A and DAF-B observed during purification.