This outcome was accomplished by transgenic intrathyroidal expression of the hTSHR A-subunit in NOD.H2<sup>h4</sup> mice that are genetically predisposed to develop thyroiditis but, without the transgene, do not generate TSHRAb.
In this study, we found that Th17 cells were significantly increased with a high expression of miR-326 in an iodine-induced thyroiditisNOD.H-2<sup>h4</sup> mouse model.
We observed evident thyroiditis in the high‑iodine-treated NOD.H-2<sup>h4</sup> mice, while mice in the other three groups did not develop thyroiditis.
GL effectively attenuated thyroiditis in the iodine-induced NOD.H-2<sup>h4</sup> mice via a molecular mechanism related to the inhibition of TLR2-HMGB1 signaling.
In the field of autoimmune thyroiditis, NOD.H2(h4) mice have attracted significant and increasing attention since they not only develop spontaneous disease but they present thyroiditis with accelerated incidence and severity if they ingest iodide through their drinking water.
In animal studies, we have transferred thyroiditis to naive BALBc and NOD mice, using T cells primed to the human TSHR, either using the receptor expressed as a bacterial fusion protein or by genetic immunization.