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Thyroid follicular cell function after non-lethal complement membrane attack.

A P Weetman1, M Freeman, B P Morgan

  • 1Department of Medicine, University of Cambridge Clinical School, England, UK.

Clinical and Experimental Immunology
|October 1, 1990
PubMed
Summary
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Complement activation and membrane attack complexes (MAC) impact thyroid function in autoimmune thyroiditis. Non-lethal MACs impair thyroid cell response to TSH and antibodies, potentially worsening disease.

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Terminal complement complexes are found around thyroid follicles in Graves' disease and Hashimoto's thyroiditis.
  • Elevated complement complex concentrations in patient sera suggest a role in autoimmune thyroiditis.

Purpose of the Study:

  • To investigate the role of complement activation and membrane attack complexes (MAC) in autoimmune thyroiditis using cultured human and rat thyroid cells.
  • To determine the effects of non-lethal MAC formation on thyrocyte function and inflammatory responses.

Main Methods:

  • Cultured human and rat thyrocytes were exposed to homologous and heterologous complement.
  • Non-lethal MAC formation was induced using reactive lysis or classical pathway activation.
  • Cellular responses, including cAMP production and reactive oxygen metabolite generation, were measured.

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Main Results:

  • Thyrocytes were resistant to homologous complement lysis but sensitive to heterologous complement.
  • Non-lethal MAC formation significantly reduced cAMP production in response to TSH and thyroid-stimulating antibodies.
  • Thyroid cells recovered rapidly from complement attack.
  • Non-lethal MAC formation induced reactive oxygen metabolite production in some thyroid cell preparations.

Conclusions:

  • Sub-lethal complement attack may exacerbate hypothyroidism in Hashimoto's thyroiditis or counteract TSH receptor stimulation in Graves' disease.
  • Reactive oxygen metabolite production during complement attack could enhance intra-thyroidal inflammation.
  • The anti-inflammatory effects of anti-thyroid drugs may be partly due to oxygen radical scavenging.