Increase of Circulating CXCL9 and CXCL11 Associated with Euthyroid or Subclinically Hypothyroid Autoimmune Thyroiditis

Abstract

We first show that circulating CXCL9 and CXCL11 are increased in patients with thyroiditis and hypothyroidism and are related to each other. These results underline the importance of a Th1 immune attack in the initiation of AIT.

Increase of Interferon-γ Inducible CXCL9 and CXCL11 Serum Levels in Patients with Active Graves' Disease and Modulation by Methimazole Therapy

“…Increased expression of CXCL10 and CXCL9 was also observed in thyroid tissue specimens obtained from subjects affected by AT by immunohistochemistry (11), and high levels of CXCL9 and CXCL11 have recently been shown in patients with AT, in particular in the presence of hypothyroidism (16)(17)(18). Furthermore, we have recently shown that IFN-c and TNF-a are able to induce the secretion of the CXCL9 and CXCL11 chemokines in thyrocytes and fibroblasts of patients with GD and ophthalmopathy (19)(20)(21).…”

Low levels of circulating platelet factor 4 (PF4, CXCL4) in subclinically hypothyroid autoimmune thyroiditis

“…In subsequent years, they demonstrated higher circulating levels of CXCL9, CXCL10, CXCL11 and comparable levels of CCL2 in patients with AIT than in controls or patients with nontoxic multinodular thyroid (NNT). Furthermore, they showed that CXCL9, CXCL10, CXCL11 and CCL2 were significantly higher in patients those with hypothyroidism [18][19][20]. In another study conducted by Domberg et al [21], circulating concentrations of CCL2, CCL5, CXCL9 and CXCL10 were also investigated in patients with GD, AIT and NNT.…”

IFNγ-Inducible Chemokines Decrease upon Selenomethionine Supplementation in Women with Euthyroid Autoimmune Thyroiditis: Comparison between Two Doses of Selenomethionine (80 or 160 μg) versus Placebo

“…A subgroup of chemokines, CXCL-9, -10 and -11, have been reported to be elevated in the serum of patients with AIT, especially those who are hypothyroid [12,13]. These proinflammatory cytokines are secreted upon IFNγ stimulation, potentially by both lymphocytes and thyroid follicular cells, and they may recruit activated Th1 lymphocytes to the inflammation site, thus maintaining and amplifying the autoimmune process in the thyroid [12,14,15].…”