Increased CXCL10 was significantly associated with the presence of active vasculitis in HCV-associated cryoglobulinemia, or with autoimmune thyroiditis in CHC.
A Th1 immune-preponderance has been shown in the immunopathogenesis of autoimmune thyroiditis (AT), Graves' disease (GD) and Graves' Ophthalmopathy (GO), in which the Th1-chemokines (CXCL9, CXCL10, CXCL11), and their (C-X-C)R3 receptor, have a crucial role.
We assessed the interferon (IFN)-γ-inducible protein 10 (IP-10/CXCL10) secretion by stimulating primary thyrocytes (obtained from Hashimoto's thyroiditis or from control patients) with cytokines in presence/absence of H<sub>2</sub>O<sub>2.</sub> Our results confirm: 1) the toxic effect of H<sub>2</sub>O<sub>2</sub> in primary thyrocytes that leads to an increase of the apoptosis, to a decrease of the proliferation, and to a slight reduction of cytokines-induced CXCL10 secretion; 2) the secretion of CXCL10 chemokine induced by IFN-γ + tumor necrosis factor alpha (TNF)-α has been decreased by Myo + Ins, both in presence or absence of H<sub>2</sub>O<sub>2</sub>; 3) no effect has been shown by the treatment with Se.
A Th1 immune predominance has been shown in early PsO, and PsA, with high serum CXCL10 (Th1 prototype chemokine), overall in the presence of autoimmune thyroiditis.
Further, significantly high serum levels of CXCL10 in patients with MC + HCV compared with healthy controls were confirmed, overall in the presence of AT.
In contrast, CXCL10 levels were lower in patients with GD, but the difference was statistically significant only when compared with patients with HT (p=0.0018).
Expression of MCP-1, RANTES, MIP-1 alpha, MIP-1 beta, IP-10 and Mig was demonstrated in all Hashimoto's and most Graves' thyroid specimens but very little expression was detected in the nonautoimmune goitre samples.