Ablation of IFN-γ, or IL-17, but not IL-4, in NOD.H2h4 mice demonstrated resistance to both thyroiditis and the generation of anti-thyroglobulin autoantibodies, indicating that both Th1 and Th17 cells are the T-cell subsets critical for the pathogenesis of iodine-induced AIT in these mice [80,81]. This evidence concerns the gene IL17A and thyroiditis.