The implication of Th17 cells, the proportion of which is increased in the blood of GCA patients and that infiltrate GCA arteries [35,36,37], contrasts with a quantitative defect of circulating Treg (CD4+CD25highFoxP3+) and the low expression of FoxP3 in the arteries of GCA patients [36,101]. The gene discussed is FOXP3; the disease is temporal arteritis.