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Endocrine Abstracts (2012) 29 S18.3

ICEECE2012 Symposia Molecular mechanisms in autoimmune thyroid disease (3 abstracts)

Regulatory cells, Th17 lymphocytes, and dendritic cells in autoimmune thyroid disease

M. Marazuela


Hospital de la Princesa, Madrid, Spain.


Human autoimmune thyroid diseases (AITD), mainly including Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), are characterized by reactivity to self-thyroid antigens. Regulatory T cells have an important role in immune tolerance to self-antigens. We have reported that different regulatory T cell subsets are abundant in the peripheral blood and in inflamed thyroid tissue in AITD and are able to synthesize the immunoregulatory cytokines IL-10 and TGF-beta. However, they are apparently unable to downmodulate the autoimmune response and the tissue damage seen in AITD.

Since there is a reciprocal negative regulation between Treg and Th17 lymphocytes, we hypothesized that the defect in T regulatory cells could be related to an expansion of Th17 cells. Accordingly, we found a higher proportion of Th17 cells and raised levels of Th17 cytokines in the peripheral blood and thyroid gland from patients with AITD, mainly those with HT. Thus, our data suggest that Th17 may have a relevant role in the inflammatory phenomenon and tissue destruction seen in HT.

Dendritic cells (DCs) bear the great responsibility of discerning whether a particular antigen must be interpreted as harmful or innocuous; whether specific T cells must develop to self-reactive T cells or to regulatory T cells. In humans, two subtypes of DCs: myeloid (mDCs) and plasmacytoid (PDCs) have been reported, each one with different phenotype and function. We have studied the phenotype and function of both DCs (mDCs and PDCs) including the expression and function of inhibitory receptors. We have found phenotypic and functional abnormalities in DCs from peripheral blood and the thyroid gland in patients with AITD that point to a role in the amplification and/or perpetuation of the immune process. These findings add additional elements to the complex pathogenesis of AITD.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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