Hashimoto's thyroiditis pathophysiology: Difference between revisions
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*A family history of thyroid disorders is common, with HLA-B* 46:01 confers an increased risk of HT developing in Han Chinese children. The genes implicated vary in different groups and the incidence is increased in patients with chromosomal disorders, like[[Down syndrome|Down's]]. | *A family history of thyroid disorders is common, with HLA-B* 46:01 confers an increased risk of HT developing in Han Chinese children. The genes implicated vary in different groups and the incidence is increased in patients with chromosomal disorders, like[[Down syndrome|Down's]]. | ||
==References== | ==References== | ||
Revision as of 18:21, 17 July 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Hashimoto's thyroiditis (HT) is characterized by Lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens.The pathogenesis is not yet completely understood. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones.
Pathophysiology
Cellular and humoral immunity is thought to be involved in the pathophysiology of Hashimoto's thyroiditis:[1]
Cellular immunity
- Defects in T suppressor cell response to thyroid-specifc antigens in autoimmune hypothyroidism resulting in failure of T suppressor function.
- Regulatory T cells like T suppressor cells also dampen the immune response. Regulatory T cells are high in CD25 expression and have altered activity in Hashimoto thyroiditis.
- CD4+ cells are less sensitive to the inhibitory effect of TGFβ in Hashimoto thyroiditis.
- There is an increased number of follicular helper T cells in patients Hashimoto's thyroiditis, which correlates with thyroid-specifc antibody levels.
Humoral immunity
- Patients with Hashimoto thyroiditis have positive antibodies against thyroglobulin (TG) and Thyroid peroxidase (TPO).
- Recently, a distinct variant of HT has been documented where the thyroid gland is infiltrated with IgG4-positive cells.
- Thyroid hormone receptor antibodies might be involved in the disease presentation as sometimes thyroiditis presents as hyperthyroidism. The balance between the thyroid stimulating antibodies (TSAb) and thyroid blocking antibodies (TBAb) explains the fluctuating hormone levels in patients with Hashimoto's thyroiditis. It should also be noted that thyroid stimulating antibodies (TSAb) might have a minor blocking action.
- The sodium iodide symporter (NIS) mediates iodine uptake by the thyroid gland, while pendrin is responsible for the efflux of iodine through thyroid follicles. Antibodies against NIS and pendrin are also found in Hashimoto thyroiditis (HT).
Cytokines
- Increased plasma level and expressions of IL-17 and IL-22 are seen in HT.
Micro RNA
- MicroRNAs (miRNA), which are small noncoding RNA regions, have also been implicated in the pathogenesis of thyroid immunity. In HT tissue, a decreased level of miR-155_2 and an increase in miR-200a1 was found.
Genetics
- A family history of thyroid disorders is common, with HLA-B* 46:01 confers an increased risk of HT developing in Han Chinese children. The genes implicated vary in different groups and the incidence is increased in patients with chromosomal disorders, likeDown's.
References
- ↑ Ajjan RA, Weetman AP (2015). "The Pathogenesis of Hashimoto's Thyroiditis: Further Developments in our Understanding". Horm. Metab. Res. 47 (10): 702–10. doi:10.1055/s-0035-1548832. PMID 26361257.