A study of programmed death‐1/programmed death ligand and iodine‐induced autoimmune thyroiditis in NOD.H‐2h4 mice

Abstract

AbstractExcess iodine will trigger the occurrence of autoimmune thyroiditis (AIT), and programmed death‐1 (PD‐1)/programmed death ligand (PD‐L) will also contribute to the development of AIT. The purpose of this study was to explore the role that negative regulatory signals mediated by PD‐1/PD‐L play in the development of spontaneous autoimmune thyroiditis (SAT) in NOD.H‐2h4 mice when they are exposed to iodine. Programmed death ligand 1 (PD‐L1) antibody was administered intraperitoneally to NOD.H‐2h4 mice. The relevant indicators were determined by flow cytometry, real‐time quantitative polymerase chain reaction, enzyme‐linked immunosorbent assay, immunohistochemistry, pathological hematoxylin and eosin staining, and arsenic–cerium catalytic spectrophotometry. Results showed that the level of urinary iodine, the level of thyroid lymphocyte infiltration, the level of thyroglobulin antibodies (TgAb) and interferon (IFN‐γ)/tumor necrosis factor (TNF‐α)/interleukin (IL‐2)/IL‐17, and the relative expression of PD‐1/PD‐L1/programmed death‐2 (PD‐L2) increased with the intervention of excess iodine. After the intervention of the PD‐L1 antibody, the expression of PD‐1/PD‐L1/PD‐L2 in different degrees was inhibited, but the level of thyroid lymphocyte infiltration and serum TgAb/IFN‐γ/TNF‐α/ IL‐2/IL‐17 did not decrease. Collectively, although PD‐1/PD‐L participates in the occurrence of SAT and induces inflammation, administration of the PD‐L1 antibody does not effectively improve the pathological process of SAT. More research is needed to determine whether PD‐1/PD‐L intervention can treat autoimmune thyroid disease.