Chemokines in thyroid autoimmunity

The chemokine receptor CXCR3 and its chemokines CXCL9, CXCL10, and CXCL11 are involved in the pathogenesis of autoimmune dis-eases. Th1 lymphocytes are recruited by Th1 chemokines, secreted by damaged cells. In inflamed tissues, the attracted Th1 lymphocytes induce the IFN-gamma and TNF-alpha release, that stimulates the secretion of Th1 chemokines, initiating and reiterating an amplifi-cation feedback loop. Autoimmune thyroid disorders (AITD) are the most recurrent autoimmune diseases, including Graves' disease (GD) and autoimmune thyroiditis, clinically defined by thyrotoxicosis and hypothyroidism, respectively. Graves' ophthalmopathy is one of GD extrathyroidal manifestations, occurring in similar to 30-50% of GD patients. In the early phase of AITD, the Th1 immune response is prevalent, and a following switch to a Th2 immune response has been shown in the late, inactive, phase. The reviewed data underline the importance of chemokines in thyroid autoimmunity and suggest CXCR3-receptor and its chemokines as potential targets of novel drugs for these disorders. (c) 2023 Elsevier Ltd. All rights reserved.

Automated summary

The chemokine receptor CXCR3 and its chemokines CXCL9, CXCL10, and CXCL11 play a role in the development of autoimmune diseases. Th1 lymphocytes are attracted by Th1 chemokines released by damaged cells. Inflammation leads to the release of IFN-gamma and TNF-alpha by Th1 lymphocytes, which further stimulates the secretion of Th1 chemokines, creating an amplification feedback loop. Autoimmune thyroid disorders (AITD), including Graves' disease (GD) and autoimmune thyroiditis, are the most common autoimmune diseases characterized by thyrotoxicosis and hypothyroidism. In AITD, there is a shift from Th1 immune response to Th2 immune response. The importance of chemokines in thyroid autoimmunity suggests that CXCR3 receptor and its chemokines could be potential targets for novel drugs.