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New ideas in thyroid autoimmunity.

R Pujol-Borrell, I Todd, M Londei

    Hormone Research
    |January 1, 1987
    PubMed
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    Inappropriate human leukocyte antigen (HLA) class II expression by endocrine cells in autoimmune diseases may trigger pathogenesis. Thyrocytes expressing HLA class II present autoantigens, but regulation varies, as seen in type I diabetes.

    Area of Science:

    • Immunology
    • Endocrinology
    • Autoimmune Diseases

    Background:

    • Endocrine epithelial cells typically lack human leukocyte antigen (HLA) class II expression.
    • Aberrant HLA class II expression is observed in endocrine cells during autoimmune conditions.
    • This inappropriate expression is hypothesized to facilitate autoantigen presentation, contributing to disease.

    Purpose of the Study:

    • To investigate the role of inappropriate human leukocyte antigen (HLA) class II expression in endocrine autoimmune diseases.
    • To explore the capacity of class II-positive thyrocytes to present autoantigens.
    • To examine the regulatory mechanisms of HLA class II expression in endocrine cells.

    Main Methods:

    • Analysis of human leukocyte antigen (HLA) class II expression in endocrine epithelial cells.

    Related Experiment Videos

  • Investigation of autoantigen presentation by class II-positive thyrocytes.
  • Assessment of regulatory factors (interferon-gamma, thyroid-stimulating hormone, epidermal growth factor) on thyrocyte class II expression.
  • Comparison with HLA class II expression in type I diabetes islet beta cells.

    • Main Results:

    • Class II-positive thyrocytes can present both exogenous antigenic peptides and intrinsic autoantigens to T cells.
    • Interferon-gamma induces class II expression in thyrocytes.
    • Thyroid-stimulating hormone and epidermal growth factor differentially regulate thyrocyte class II expression.
    • Islet beta cells in type I diabetes aberrantly express class II, but this is not inducible by interferon-gamma in normal cells.

    Conclusions:

    • Inappropriate human leukocyte antigen (HLA) class II expression by endocrine cells is implicated in autoimmune pathogenesis.
    • Thyrocytes can present autoantigens, highlighting a potential mechanism in autoimmune thyroid disease.
    • Regulatory pathways for HLA class II expression are complex and cell-type specific, as evidenced by type I diabetes findings.