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Related Experiment Video

Updated: Oct 2, 2025

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Diversity of complement activation in different thyroid diseases.

Chenxu Zhao1, Yang Yu2, Jumei Liu3

  • 1Department of Endocrinology, Peking University First Hospital, No. 8 Xi Shi Ku Street, Xicheng District, Beijing 100034, China; Department of Endocrinology, Hebei Medical University First Affiliated Hospital, No. 89 Dong Gang Road, Yuhua District, Shijiazhuang, China.

International Immunopharmacology
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Summary

Complement is overactivated in Hashimoto

Keywords:
ComplementGraves’ diseaseHashimoto’s thyroiditisPapillary thyroid cancer

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Area of Science:

  • Immunology
  • Endocrinology
  • Pathology

Background:

  • The complement system plays a crucial role in innate immunity.
  • Dysregulation of the complement system is implicated in various autoimmune and neoplastic diseases.
  • Thyroid autoimmune diseases and thyroid cancer involve complex inflammatory processes.

Purpose of the Study:

  • To investigate complement component expression in thyroid tissues and serum of patients with Hashimoto's thyroiditis (HT), Graves' disease (GD), and papillary thyroid cancer (PTC).
  • To compare complement activation profiles across these thyroid conditions and healthy controls.

Main Methods:

  • Immunohistochemistry (IHC) was used to examine complement component deposition and regulatory protein expression in thyroid tissues.
  • Enzyme-linked immunosorbent assays (ELISAs) were employed to measure serum levels of complement components.
  • Patients with HT, GD, PTC, and healthy donors (HD) were included in the study.

Main Results:

  • Membrane attack complex (MAC) deposition was observed in thyroid tissues of HT, GD, and PTC patients, but not in controls.
  • Significantly higher levels of MBL, Bb, C4d, C3d, and MAC were found in thyroid tissues of HT and PTC groups compared to controls.
  • Serum levels of Bb, C4d, C3a, and soluble C5b-9 (sC5b-9) were elevated in HT, GD, and PTC patients compared to HDs.

Conclusions:

  • Complement system is overactivated in Hashimoto's thyroiditis and papillary thyroid cancer, but not in Graves' disease.
  • All three complement pathways (classical, lectin, and alternative) are activated in HT.
  • The mannose-binding lectin (MBL) and alternative pathways are activated in PTC, suggesting distinct roles in disease pathogenesis.