The results indicate that CCL2 can be produced by thyroid follicular cells themselves under the influence of cytokines such as IFN-γ or TNF-α, which are released by activated Th1 lymphocytes and confirm the hypothesis that autoimmune disorders in thyroid of GD patients evolve from an initial Th1 phase to a later Th2 prevalent immune response. This evidence concerns the gene TNF and autoimmune disease.