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[Animal models in lupus].

O Meyer

    Revue Du Rhumatisme Et Des Maladies Osteo-Articulaires
    |December 1, 1981
    PubMed
    Summary
    This summary is machine-generated.

    Spontaneous animal models reveal autoimmune disease mechanisms, highlighting intrinsic B lymphocyte hyperactivity and T lymphocyte dysregulation. These models aid in understanding lupus pathogenesis and genetic control, suggesting potential viral roles.

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    Area of Science:

    • Immunology
    • Autoimmune Diseases
    • Veterinary Pathology

    Background:

    • Spontaneous animal models offer insights into complex autoimmune diseases like lupus.
    • Understanding the mechanisms of auto-antibody production and immune complex-mediated glomerulonephritis is crucial.

    Purpose of the Study:

    • To elucidate the intermediary mechanisms in the development of lupoid diseases using animal models.
    • To investigate the roles of T and B lymphocytes in the pathogenesis of autoimmune disorders.
    • To explore the genetic and potential infectious factors contributing to lupus.

    Main Methods:

    • Studying spontaneous animal models of lupoid disease, including various murine strains (NZB, NZB X NZW F1, MRL/1 pr, B X SB).
    • Analyzing immune regulation, T lymphocyte subsets (activating and suppressing), and B lymphocyte activity.

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  • Investigating canine lupus and Aleutian mink disease to identify potential transmittable agents.

    • Main Results:

    • Animal models demonstrate the importance of intrinsic B lymphocyte hyperactivity, alongside thymic deficiency-related immune dysregulation.
    • The combined disturbance of T and B lymphocytes appears necessary for disease development in specific mouse models (NZB, NZB X NZW F1).
    • Diverse lymphocytic disturbances across different murine models can lead to auto-antibody production, indicating varied pathogenic pathways.

    Conclusions:

    • Spontaneous animal models are invaluable for understanding lupus pathogenesis, immune regulation, and auto-antibody production.
    • Intrinsic B lymphocyte hyperactivity and T lymphocyte dysregulation are key factors in lupoid disease development.
    • Further research into genetic factors and potential viral agents is warranted for a comprehensive understanding and control of autoimmune diseases.