The chemokine (C-X-C motif) ligand 10 (CXCL10, also called IP-10) was initially identified as a chemokine that is induced by interferon (IFN)-γ. CXCL10 exerts its function through binding to chemokine (C-X-C motif) receptor 3 (CXCR3). CXCL10 and its receptor, CXCR3, appear to contribute to the pathogenesis of many autoimmune diseases, organ specific (such as type 1 diabetes, Graves' disease and ophthalmopathy), or systemic (such as systemic lupus erythematosus, mixed cryoglobulinemia, Sjogren syndrome, or systemic sclerosis). The secretion of CXCL10 by CD4+, CD8+, and natural killer is dependent on IFN-γ. Under the influence of IFN-γ, CXCL10 is secreted by thyrocytes. Determination of high level of CXCL10 in peripheral fluids is therefore a marker of a T helper 1 orientated immune response. High levels of circulating CXCL10, have been shown in patients with autoimmune thyroiditis (AT). Among patients with AT, CXCL10 levels were significantly higher in those with a hypoechoic ultrasonographic pattern, that is a sign of a more severe lympho-monocytic infiltration, and in those with hypothyroidism. For these reasons it has been postulated that CXCL10 could be a marker of a stronger and more aggressive inflammatory response in the thyroid, subsequently leading to thyroid destruction and hypothyroidism. Further studies are needed to investigate whether CXCL10 is a novel therapeutic target in AT.

[CXCR3 and CXCL10 in autoimmune thyroiditis] / Ruffilli, I; Ferrari, Silvia Martina; Colaci, Michele; Ferri, Clodoveo; Politti, U; Antonelli, A; Fallahi, P.. - In: LA CLINICA TERAPEUTICA. - ISSN 1972-6007. - ELETTRONICO. - 165:(2014), pp. 237-242. [10.7417/CT.2014.1727]

[CXCR3 and CXCL10 in autoimmune thyroiditis]

FERRARI, Silvia Martina;COLACI, Michele;FERRI, Clodoveo;
2014

Abstract

The chemokine (C-X-C motif) ligand 10 (CXCL10, also called IP-10) was initially identified as a chemokine that is induced by interferon (IFN)-γ. CXCL10 exerts its function through binding to chemokine (C-X-C motif) receptor 3 (CXCR3). CXCL10 and its receptor, CXCR3, appear to contribute to the pathogenesis of many autoimmune diseases, organ specific (such as type 1 diabetes, Graves' disease and ophthalmopathy), or systemic (such as systemic lupus erythematosus, mixed cryoglobulinemia, Sjogren syndrome, or systemic sclerosis). The secretion of CXCL10 by CD4+, CD8+, and natural killer is dependent on IFN-γ. Under the influence of IFN-γ, CXCL10 is secreted by thyrocytes. Determination of high level of CXCL10 in peripheral fluids is therefore a marker of a T helper 1 orientated immune response. High levels of circulating CXCL10, have been shown in patients with autoimmune thyroiditis (AT). Among patients with AT, CXCL10 levels were significantly higher in those with a hypoechoic ultrasonographic pattern, that is a sign of a more severe lympho-monocytic infiltration, and in those with hypothyroidism. For these reasons it has been postulated that CXCL10 could be a marker of a stronger and more aggressive inflammatory response in the thyroid, subsequently leading to thyroid destruction and hypothyroidism. Further studies are needed to investigate whether CXCL10 is a novel therapeutic target in AT.
165
237
242
[CXCR3 and CXCL10 in autoimmune thyroiditis] / Ruffilli, I; Ferrari, Silvia Martina; Colaci, Michele; Ferri, Clodoveo; Politti, U; Antonelli, A; Fallahi, P.. - In: LA CLINICA TERAPEUTICA. - ISSN 1972-6007. - ELETTRONICO. - 165:(2014), pp. 237-242. [10.7417/CT.2014.1727]
Ruffilli, I; Ferrari, Silvia Martina; Colaci, Michele; Ferri, Clodoveo; Politti, U; Antonelli, A; Fallahi, P.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1061022
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