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Role of late complement components in experimental autoimmune thyroiditis

K Inoue1, N Niesen, G Biesecker

  • 1Department of Microbiology, State University of New York, Buffalo 14214.

Clinical Immunology and Immunopathology
|January 1, 1993
PubMed
Summary
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The terminal complement complex (TCC) is crucial for severe experimental autoimmune thyroiditis (EAT) in rabbits. However, EAT can still develop, albeit less severely, without TCC, indicating its partial role.

Area of Science:

  • Immunology
  • Pathogenesis of Autoimmune Diseases

Background:

  • Experimental autoimmune thyroiditis (EAT) is a model for human autoimmune thyroid diseases.
  • The role of the terminal complement complex (TCC) in EAT pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the necessity of the terminal complement complex (TCC) for the development of experimental autoimmune thyroiditis (EAT) in rabbits.
  • To evaluate the impact of C6 deficiency on EAT severity and pathogenesis.

Main Methods:

  • Induction of EAT in normocomplementemic (NC) and C6-deficient (C6-D) rabbits using homologous thyroid extract.
  • Assessment of thyroiditis severity, cellular infiltrates, and follicular destruction.
  • Immunohistological analysis for complement component deposition (C3, C6, MAC) and immunoglobulins (IgG).

Related Experiment Videos

  • Evaluation of T-cell activity in C6-D rabbits by inducing experimental autoallergic encephalomyelitis.

    • Main Results:

    • Rabbits deficient in C6 (C6-D) exhibited significantly reduced severity of EAT compared to normocomplementemic (NC) rabbits.
    • NC rabbits showed severe, diffuse thyroiditis with extensive follicular destruction, while C6-D rabbits had minimal, focal thyroiditis.
    • Deposits of IgG and C3 were observed in both groups, but C6 and MAC deposition was restricted to NC rabbits.
    • C6-D rabbits maintained normal T-cell activity, indicating the impairment was specific to complement-mediated pathways.

    Conclusions:

    • The terminal complement complex (TCC) is necessary for the full development of severe experimental autoimmune thyroiditis (EAT).
    • A reduced form of EAT can develop independently of TCC, suggesting alternative pathogenic mechanisms.
    • C6 deficiency significantly impairs EAT development in rabbits, highlighting the role of complement in this autoimmune condition.
    • Findings may offer insights into the pathogenesis of human autoimmune thyroiditis, such as Hashimoto's thyroiditis, where TCC deposits have been observed.