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Related Experiment Videos

A Modifying Autoantigen in Graves' Disease.

Rauf Latif1,2, Mihaly Mezei3, Syed A Morshed1,2

  • 1Thyroid Research Unit, Icahn School of Medicine at Mount Sinai, New York, New York.

Endocrinology
|March 2, 2019
PubMed
Summary

A novel thyroid receptor variant, TSHRv1.3, is expressed in Graves' disease and can bind antibodies and TSH. This variant inhibits TSHR signaling and shows antigenicity, suggesting a role in thyroid pathophysiology.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Immunology

Background:

  • The TSH receptor (TSHR) is a key autoantigen in Graves' disease (GD).
  • Alternative splicing of TSHR mRNA generates multiple receptor isoforms, including the abundant TSHRv1.3.
  • The functional and pathological significance of TSHRv1.3 remains largely unexplored.

Purpose of the Study:

  • To investigate the structural integrity, binding capabilities, and functional role of the TSHRv1.3 isoform.
  • To assess the antigenicity of TSHRv1.3 in patients with Graves' disease.
  • To explore the potential of TSHRv1.3 as an autoantigen and its modulation of thyroid pathophysiology.

Main Methods:

  • In silico modeling and tissue expression profiling of TSHRv1.3.
  • Cloning and expression of TSHRv1.3 in mammalian cells.

Related Experiment Videos

  • Immunoprecipitation, ELISA, and cAMP generation assays.
  • Studies using double-transfected cells to induce apoptosis and assess TSHRv1.3 release.

    • Main Results:

    • In silico modeling confirmed the structural integrity and TSH-binding potential of TSHRv1.3.
    • TSRv1.3 is widely expressed, particularly in thyroid and immune tissues.
    • TSRv1.3 binds both TSH and TSHR-stimulating antibodies.
    • TSRv1.3 demonstrated a dose-dependent inhibition of TSHR-mediated cAMP signaling.
    • A high percentage of GD patients showed positive reactivity to TSHRv1.3 peptides.
    • Cell stress and apoptosis induced the release of TSHRv1.3.

    Conclusions:

    • TSHv1.3 is a structurally sound, functional TSHR isoform with significant expression in relevant tissues.
    • TSHv1.3 acts as an autoantigen in Graves' disease and can modulate TSHR signaling.
    • The release of TSHRv1.3 during cell apoptosis suggests a mechanism for its involvement in autoimmune thyroid disease pathogenesis.