IMR Press / FBL / Volume 11 / Issue 2 / DOI: 10.2741/1876

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Tolerance to autoimmune thyroiditis: CD4+CD25+ regulatory T cells influence susceptibility but do not supersede MHC class II restriction

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1 Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA
Front. Biosci. (Landmark Ed) 2006, 11(2), 1234–1243;
Published: 1 May 2006

Murine experimental autoimmune thyroiditis (EAT), a model of Hashimoto's thyroiditis, has served for more than three decades as a prototypical model of T cell-mediated autoimmunity. Early investigations demonstrated a clear correlation between genetic factors, particularly the H2A locus of the MHC class II region, and susceptibility to autoimmune thyroiditis. Early studies also demonstrated that susceptibility to EAT induction could be modulated by manipulation of circulating levels of thyroglobulin (Tg), the principal thyroid antigen, resulting in the strengthening of self-tolerance. This antigen-specific induced tolerance is mediated by thymus-derived cells, and subsequent investigations revealed that the suppressive function is located in the CD4+CD25+ T cell subset, similar to findings in other models. We have demonstrated that these CD4+CD25+ regulatory T cells (Treg) influence susceptibility to thyroiditis in naive, as well as mTg-tolerized mice. Here, we describe the influence of both Treg and MHC class II haplotype, independently, as well in combination, and describe our recent utilization of MHC class II transgenic mice to directly compare the extent of their influences.

Immune response
Autoimmune Thyroiditis
CD4+ CD25+ T cells
MHC class II
regulatory T cells
Self Tolerance
Acquired Tolerance
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