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

Excess 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-& gamma;)/tumor necrosis factor (TNF-& alpha;)/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-& gamma;/TNF-& alpha;/ 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.

Automated summary

Excess iodine triggers autoimmune thyroiditis (AIT), while programmed death-1 (PD-1)/programmed death ligand (PD-L) also contribute to AIT development. This study aimed to explore the role of negative regulatory signals mediated by PD-1/PD-L in spontaneous autoimmune thyroiditis (SAT) development in NOD.H-2h4 mice exposed to iodine. NOD.H-2h4 mice were administered intraperitoneal PD-L1 antibody. Various indicators were determined, and results showed increased urinary iodine level, thyroid lymphocyte infiltration, thyroglobulin antibodies (TgAb), interferon (IFN-γ)/tumor necrosis factor (TNF-α)/interleukin (IL-2)/IL-17 levels, and expression of PD-1/PD-L1/programmed death-2 (PD-L2) with excess iodine intervention. Inhibition of PD-1/PD-L1/PD-L2 expression, however, did not decrease thyroid lymphocyte infiltration and serum TgAb/IFN-γ/TNF-α/IL-2/IL-17 levels. Further research is needed to determine if PD-1/PD-L intervention can effectively treat autoimmune thyroid disease.