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Murine lupus.

S K Datta

    Methods in Enzymology
    |January 1, 1988
    PubMed
    Summary
    This summary is machine-generated.

    In lupus nephritis mice, anti-DNA antibodies change to become pathogenic. Crossing normal mice with autoimmune strains activates these antibodies, leading to severe kidney disease.

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    Area of Science:

    • Immunology
    • Autoimmunity
    • Nephrology

    Background:

    • Lupus nephritis is characterized by pathogenic anti-DNA antibodies.
    • These antibodies undergo qualitative changes, including IgG switch and increased cationic charge.
    • The genetic basis for pathogenic anti-DNA antibodies involves specific idiotypes.

    Purpose of the Study:

    • To investigate the genetic encoding and expression of pathogenic anti-DNA idiotypes.
    • To understand the role of immunoregulation defects in the development of lupus nephritis.
    • To explore the mechanism by which dormant idiotypes become pathogenic.

    Main Methods:

    • Utilizing mouse models, specifically SWR (normal) and NZB (autoimmune) strains.
    • Cross-breeding normal mice with autoimmune strains to generate F1 hybrids.

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  • Analyzing anti-DNA antibody characteristics (e.g., IgG switch, cationic charge) in different mouse models.

    • Main Results:

    • Pathogenic anti-DNA idiotypes can be encoded by genes present in normal mouse strains (SWR).
    • These idiotypes remain dormant in normal mice but are expressed in F1 hybrids when crossed with autoimmune strains (NZB).
    • Defects in immunoregulation in F1 hybrids lead to the expression of pathogenic idiotypes.

    Conclusions:

    • Genetic predisposition for pathogenic anti-DNA antibodies exists in normal mouse strains.
    • Autoimmune strain background and compromised immunoregulation are critical for the activation and pathogenicity of these antibodies.
    • This mechanism contributes to the development of lethal glomerulonephritis in lupus nephritis models.