Estrogen receptor β activation stimulates the development of experimental autoimmune thyroiditis through up-regulation of Th17-type responses.

Clinical Immunology : the Official Journal of the Clinical Immunology Society
Juan QinWeiping Teng

Abstract

Estrogens play important roles in autoimmune thyroiditis, but it remains unknown which estrogen receptor (ER) subtype mediates the stimulatory effects. Herein we treated ovariectomized mice with ERα or ERβ selective agonist followed by thyroglobulin-immunization to induce experimental autoimmune thyroiditis (EAT), and observed the aggravation of EAT after diarylpropionitrile (DPN, ERβ selective agonist) administration. The mRNA levels of interleukin(IL)-17A, IL-21 and RORγt and percentages of T helper (Th) 17 cells were up-regulated in the splenocytes of DPN-treated mice. Activated ERβ was found directly binding to IL-17A and IL-21 gene promoters, and also indirectly promoting IL-21 and RORγt gene transcription through interaction with NF-κB. The expressions of co-stimulatory molecules were increased on antigen-presenting cells (APCs) after DPN administration. It suggests that ERβ is the predominant ER subtype responsible for EAT development, and its activation may enhance Th17-type responses through genomic pathways and alteration of APCs' activities.

Citations

Sep 25, 2019·International Journal of Molecular Sciences·Naoko KandaHidehisa Saeki
Feb 23, 2020·American Journal of Physiology. Heart and Circulatory Physiology·Lijuan JiaoHong Sun
Oct 4, 2020·Nature Reviews. Rheumatology·Maurizio Cutolo, Rainer H Straub
Sep 17, 2021·Reviews in Endocrine & Metabolic Disorders·Kardalas EfstratiosMastorakos George

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