MIG in autoimmune thyroiditis: review of the literature

doi: 10.7417/CT.2019.2151

  • M. Pezzano Department of Clinical and Experimental Medicine, University of Pisa, Italy

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.

Published
2019-07-12
How to Cite
PEZZANO, M.. MIG in autoimmune thyroiditis: review of the literature. La Clinica Terapeutica, [S.l.], v. 170, n. 4, p. e295 - e300, july 2019. ISSN 1972-6007. Available at: <http://www.clinicaterapeutica.it/ojs/index.php/ClinicaTerapeutica/article/view/457>. Date accessed: 22 oct. 2019.