IL-6, which is produced in GCA lesions [98] and the concentration of which in the serum correlates with disease activity [7,36], physiologically controls the Th17/Treg balance since IL-6 and transforming growth factor-beta (TGF-β) trigger Th17 polarization, whereas TGF-β alone leads to the generation of Treg [102]. This evidence concerns the gene TGFB1 and temporal arteritis.