Article ; Online: MIG in autoimmune thyroiditis: review of the literature.
2019 Volume 170, Issue 4, Page(s) e295–e300
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 ... ...
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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MeSH term(s) | Aged ; Animals ; Chemokine CXCL9/immunology ; Hashimoto Disease/immunology ; Humans ; Interferon-gamma ; Receptors, CXCR3/immunology ; Th1 Cells/immunology |
Chemical Substances | CXCR3 protein, human ; Chemokine CXCL9 ; Receptors, CXCR3 ; Interferon-gamma (82115-62-6) |
Language | English |
Publishing date | 2019-07-15 |
Publishing country | Italy |
Document type | Journal Article ; Review |
ZDB-ID | 123320-8 |
ISSN | 1972-6007 ; 0009-9074 |
ISSN (online) | 1972-6007 |
ISSN | 0009-9074 |
DOI | 10.7417/CT.2019.2151 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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