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The chemokine receptor CXCR3 and its chemokines CXCL9, CXCL10, and CXCL11 are involved in the pathogenesis of autoimmune diseases. 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 amplification 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 ~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., Competing Interests: Conflict of interest statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Since the beginning of the pandemic, numerous risk factors have been associated with SARS-CoV-2 infection and COVID-19 outcomes, such as older age, male sex, and the presence of comorbidities, such as hypertension, obesity, and diabetes. Preliminary data also suggest epidemiological association between SARS-CoV-2 infection and systemic autoimmune disease. For this reason, we investigated if patients affected by autoimmune thyroid disorders (AITD) are at risk of developing SARS-CoV-2 infection or COVID-19 disease. From April to September 2020, we have conducted a telephone survey that included 515 consecutive unselected patients with known thyroid disorders, of which 350 were affected by AITD. All 11 definitive diagnosis of COVID-19 (def-sympt-COVID-19) belonged to the AITD group, while the rest 14 cases highly suspected for COVID-19 (suspect-sympt-COVID-19) were equally detected in both group (7 in AITD and 7 in not-AITD). The overall prevalence of symptomatic COVID-19 (def-sympt-COVID-19 + suspect-sympt-COVID-19), recorded in the 350 AITD population was statistically significant higher compared to that reported in the Italian and Tuscan general population at the same time period of the present survey (18/350 = 5.14% vs 516/100000 = 0.51% [p < 0.001; OR = 10.45, 95% CI 6.45-16.92] and vs 394/100000 = 0.39% [p < 0.001; OR = 13.70, 95% CI 8.44-22.25], respectively). Therefore, our results suggest a higher prevalence of SARS-CoV-2 infection and COVID-19 disease in patients with AITD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Graves' disease (GD) is the most common cause of hyperthyroidism in developed Countries. It is more common between 30 and 60 years; 5-10 times more frequent in women. The genetic predisposition accounts for 79% of the risk for GD, while environmental factors for 21%. About 70% of genes associated with autoimmune thyroid disorders (AITD) are implicated in T-cell function. Among GD endogenous factors, estrogens, X-inactivation and microchimerism are important. Among environmental risk factors, smoking, iodine excess, selenium and vitamin D deficiency, and the occupational exposure to Agent Orange have been associated with GD. Many studies showed that HCV is associated with thyroid autoimmunity and hypothyroidism, in patients with chronic HCV hepatitis (CHC); a significant link has been shown also between HCV-related mixed cryoglobulinemia and risk for GD. Moreover, IFN-α-treated CHC patients develop GD more frequently. Novel studies are needed about possible risk factors to reduce the occurence of GD in West Countries., Competing Interests: Declaration of Competing Interest The Authors have nothing to declare., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Graves' disease (GD) is characterized by thyrotoxicosis, caused by the presence of circulating thyroid stimulating antibodies (TSAb), that are determinant also in the pathogenesis of its extrathyroidal manifestations [Graves' ophthalmopathy (GO), pretibial myxedema]. T helper (Th)1 immune response prevails in the immune-pathogenesis of GD and GO, during the active phase, when Th1 chemokines, and their (C-X-C)R3 receptor, play a key role. In GD, the existing treatments are not ideal for hyperthyroidism (long-term remission with anti-thyroid-drugs only in 50% of patients; while radioiodine and surgery cause hypothyroidism). In GD, antigen-specific therapy has been recently published, with the induction of T cell tolerance via an immunization by TSH-R peptides. In GO, rituximab and drugs targeting cytokines have been evaluated. Furthermore, teprotumumab (a human monoclonal anti-IGF-1R blocking antibody) showed to be very effective in GO patients. Further researches are necessary to identify novel effective therapies targeting GD, or GO., Competing Interests: Declaration of Competing Interest The Authors have nothing to declare., (Copyright © 2020 Elsevier Ltd. All rights reserved.)