IFN-γ stimulation leading to the release of CXCR3-binding chemokines from thyrocytes in turn recruits Th1 lymphocytes expressing CXCR3 and producing IFN-γ, which suggests that the interferon-γ inducible chemokines (CXCL9, CXCL10, and CXCL11) and their receptor CXCR3 play an important role in the initiation of autoimmune thyroid diseases [40]. Here, CXCL11 is linked to autoimmune thyroid disease.