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Related Experiment Videos

Graves' hyperthyroidism and the hygiene hypothesis in a mouse model.

Yuji Nagayama1, Sandra M McLachlan, Basil Rapoport

  • 1Department of Medical Gene Technology, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan. nagayama@net.nagasaki-u.ac.jp

Endocrinology
|August 17, 2004
PubMed
Summary

Infection with Mycobacterium bovis bacillus Calmette-Guerin (BCG) promotes a Th1 immune response, suppressing Graves' disease development in mice. This suggests infectious agents can influence autoimmune thyroid disease independently of Th1/Th2 balance shifts.

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Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • Graves' hyperthyroidism is an autoimmune disorder driven by TSH receptor (TSHR) antibodies.
  • Disease development is influenced by genetic and environmental factors.
  • Previous studies showed helminth infection suppressed T helper cell type 1 (Th1)-mediated anti-TSHR responses.

Purpose of the Study:

  • To investigate the effect of Mycobacterium bovis bacillus Calmette-Guerin (BCG) infection on Graves' disease development.
  • To determine if BCG influences the TSHR-specific immune response phenotype.

Main Methods:

  • Mice were infected with M. bovis BCG prior to induction of a Graves' disease model.
  • Splenocytes were stimulated with TSHR antigen in vitro.
  • Cytokine production (interferon-gamma, IL-10) was measured to assess Th1/Th2 responses.

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Main Results:

  • BCG infection shifted the TSHR-specific immune response towards a Th1 phenotype.
  • Enhanced secretion of Th1 cytokine interferon-gamma and impaired production of Th2 cytokine IL-10 were observed.
  • BCG infection significantly suppressed Graves' disease induction in the mouse model.

Conclusions:

  • M. bovis BCG infection promotes a Th1-polarized immune response.
  • BCG suppresses the development of Graves' disease, supporting the hygiene hypothesis.
  • Some infectious pathogens may influence autoimmune disease regardless of Th1/Th2 balance modulation.