IL-17 would exert function to the pathogenesis of AITD by many ways: caused thyroid follicular cell produced more proinflammatory cytokine such as IL-6/IL-8/ICAM-1 etc., so that keeps synthesizing triiodothyronine constantly and inflammation fibrosis occurring; raised thyrocytes surface MHCA antigens contents as stimulating neuters’ population and matured for maintaining immune disorder through coordinating working with T cells activated, respectively; displayed cooperative inflamation stimulating effect on local site with IL-1b and TNF-a to amplify injury extent and tissues damaged. This evidence concerns the gene CXCL8 and immune system disorder.