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Related Experiment Videos

Abnormal lymphocyte function in scleroderma: a study on identical twins.

M M Dustoor, M M McInerney, D J Mazanec

    Clinical Immunology and Immunopathology
    |July 1, 1987
    PubMed
    Summary

    Identical twins discordant for scleroderma revealed immune system differences. The affected twin showed impaired T-cell function but enhanced T-helper activity, suggesting non-genetic factors in scleroderma pathogenesis.

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    Area of Science:

    • Immunology
    • Rheumatology
    • Genetics

    Background:

    • Scleroderma is an autoimmune disease characterized by fibrosis and vascular abnormalities.
    • The genetic basis of scleroderma is not fully understood, with environmental factors also implicated.
    • Studying identical twins discordant for scleroderma offers a unique model to investigate genetic versus environmental influences.

    Purpose of the Study:

    • To investigate immunologic differences between identical twins discordant for scleroderma.
    • To determine the role of genetic factors in the observed immunologic abnormalities in scleroderma.
    • To explore potential non-genetic contributors to scleroderma pathogenesis.

    Main Methods:

    • Comparative immunologic assays were performed on blood samples from affected and unaffected identical twins.

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  • T-cell subset analysis (T4 helper/inducer, T8 suppressor/cytotoxic) was conducted.
  • T-cell responsiveness to mitogens and allogeneic/autologous stimuli was assessed.
  • Pokeweed mitogen-induced IgM synthesis and T-cell helper activity were measured.
  • Collagen synthesis by normal fibroblasts treated with patient-derived mononuclear cell supernatants was evaluated.

    • Main Results:

    • The affected twin exhibited a low absolute T-cell count, reduced T4 helper/inducer cells, and increased T8 suppressor/cytotoxic cells.
    • T cells from the affected twin showed poor responses to mitogens and allogeneic/autologous stimuli.
    • Markedly enhanced T-cell helper activity for pokeweed mitogen-induced IgM synthesis was observed in the affected twin.
    • Supernatants from activated mononuclear cells of the affected twin significantly increased collagen synthesis in normal fibroblasts.
    • The unaffected twin demonstrated normal responses across all immunologic assays.

    Conclusions:

    • The immunologic defects observed in scleroderma are not solely determined by genetic factors.
    • Specific T-cell abnormalities and enhanced B-cell helper function may contribute to scleroderma pathogenesis.
    • Environmental or acquired factors likely play a significant role in the development of scleroderma in genetically predisposed individuals.