Abstract
The monokine induced by interferon (IFN)-γ (MIG) and its receptor, the chemokine (C-X-C motif) receptor (CXCR)3, appear to contribute to the pathogenesis of autoimmune thyroiditis (AT). MIG is secreted by thyrocytes under the influence of IFN-γ. In tissue, recruited Th1 lymphocytes may be responsible for enhanced IFN-γ, which in turn stimulates MIG secretion from thyrocytes creating an amplification feedback loop, and perpetuating the autoimmune process. Circulating MIG and IFN-inducible T-cell α chemoattractant (I-TAC) levels are increased in patients with thyroiditis and hypothyroidism and are related to each other. The importance of a Th1 immune attack in the initiation of AT has been demonstrated. MIG levels were significantly higher in elder patients, or in those with a hypoechoic ultrasonographic pattern, or with hypothyroidism. In peripheral fluids, high MIG levels are considered a marker of host immune response, in particular Th1 orientated T-cells. Other studies are needed to continue to investigate the role of MIG as a novel therapeutic target in AT.
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