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Complement activation in type 1 human diabetes.

J S Sundsmo, R A Papin, L Wood

    Clinical Immunology and Immunopathology
    |May 1, 1985
    PubMed
    Summary
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    Complement activation is elevated in new-onset Type 1 diabetes, with increased C3a, C4a, and C5-AA fragments. Both classical and alternative pathways appear activated, suggesting complement

    Area of Science:

    • Immunology
    • Endocrinology
    • Diabetology

    Background:

    • Complement activation is a key immune response.
    • Dysregulation of complement may play a role in diabetes pathogenesis.
    • Specific complement fragments (C3a, C4a, C5a, Factor B, C5-AA) are markers of activation.

    Purpose of the Study:

    • To quantify complement activation in diabetic patients.
    • To investigate complement pathway involvement in Type 1 diabetes.
    • To correlate complement fragment levels with disease status.

    Main Methods:

    • Radioimmunoassays (RIA) for C3a, C4a, C5a, Factor B, and C5-AA.
    • Analysis of serum and plasma from diabetic and normal subjects.
    • Longitudinal evaluation of complement fragments in new-onset Type 1 diabetes.

    Related Experiment Videos

  • In vitro complement activation assays using rat islet cells.

    • Main Results:

    • Significantly elevated plasma C3a in new-onset Type 1 diabetes (P < 0.0005).
    • Elevated C5-AA in chronic Type 1 diabetes (P < 0.0005) and new-onset diabetes (P < 0.01).
    • Increased consumption of C3 and Factor B in vitro with new-onset diabetic sera, indicating pathway activation.

    Conclusions:

    • Complement activation fragments are generated in vivo in new-onset Type 1 diabetes.
    • Both classical and alternative complement pathways are likely activated.
    • Complement activation may contribute to the pathogenesis of Type 1 diabetes.