ABSTRACT: C-X-C chemokine receptor (CXCR)3 and its interferon(IFN)γ-dependent chemokines (CXCL10, CXCL9, CXCL11) are implicated in the immune-pathogenesis of autoimmune thyroiditis (AT), Graves disease (GD) and Graves Ophthalmopathy (GO). In tissue, recruited Th1 lymphocytes produce IFNγ, enhancing the tissue secretion of IFNγ-inducible chemokines, initiating and perpetuating the autoimmune process. Patients with AT (with hypothyroidism), and with GO and GD, particularly in the active phase, have high IFNγ-inducible chemokines. Peroxisome proliferator-activated receptor (PPAR)γ or -α agonists and methimazole exert an immune-modulation on CXCR3 chemokines in AT, GD and GO. Other studies are ongoing to evaluate new molecules acting as antagonists of CXCR3, or blocking CXCL10, in Hashimoto thyroiditis (HT), GD and GO. Recently, novel molecules targeting the various agents involved in the pathogenesis of GO, such as rituximab, have been proposed as an alternative to corticosteroids. However, randomized and controlled studies are needed to generalize these interesting results.

Novel Therapies for Thyroid Autoimmune Diseases / Fallahi, Poupak; Ferrari, Silvia Martina; Elia, Giusy; Nasini, Francesco; Colaci, Michele; Giuggioli, Dilia; Vita, Roberto; Benvenga, Salvatore; Ferri, Clodoveo; Antonelli, Alessandro. - In: EXPERT REVIEW OF CLINICAL PHARMACOLOGY. - ISSN 1751-2433. - 9:(2016), pp. 853-861. [10.1586/17512433.2016.1157468]

Novel Therapies for Thyroid Autoimmune Diseases

FERRARI, Silvia Martina;COLACI, Michele;GIUGGIOLI, DILIA;FERRI, Clodoveo;
2016

Abstract

ABSTRACT: C-X-C chemokine receptor (CXCR)3 and its interferon(IFN)γ-dependent chemokines (CXCL10, CXCL9, CXCL11) are implicated in the immune-pathogenesis of autoimmune thyroiditis (AT), Graves disease (GD) and Graves Ophthalmopathy (GO). In tissue, recruited Th1 lymphocytes produce IFNγ, enhancing the tissue secretion of IFNγ-inducible chemokines, initiating and perpetuating the autoimmune process. Patients with AT (with hypothyroidism), and with GO and GD, particularly in the active phase, have high IFNγ-inducible chemokines. Peroxisome proliferator-activated receptor (PPAR)γ or -α agonists and methimazole exert an immune-modulation on CXCR3 chemokines in AT, GD and GO. Other studies are ongoing to evaluate new molecules acting as antagonists of CXCR3, or blocking CXCL10, in Hashimoto thyroiditis (HT), GD and GO. Recently, novel molecules targeting the various agents involved in the pathogenesis of GO, such as rituximab, have been proposed as an alternative to corticosteroids. However, randomized and controlled studies are needed to generalize these interesting results.
2016
8-mar-2016
9
853
861
Novel Therapies for Thyroid Autoimmune Diseases / Fallahi, Poupak; Ferrari, Silvia Martina; Elia, Giusy; Nasini, Francesco; Colaci, Michele; Giuggioli, Dilia; Vita, Roberto; Benvenga, Salvatore; Ferri, Clodoveo; Antonelli, Alessandro. - In: EXPERT REVIEW OF CLINICAL PHARMACOLOGY. - ISSN 1751-2433. - 9:(2016), pp. 853-861. [10.1586/17512433.2016.1157468]
Fallahi, Poupak; Ferrari, Silvia Martina; Elia, Giusy; Nasini, Francesco; Colaci, Michele; Giuggioli, Dilia; Vita, Roberto; Benvenga, Salvatore; Ferri, Clodoveo; Antonelli, Alessandro
File in questo prodotto:
File Dimensione Formato  
Fallahi Exp Rev Clin Pharm 2016.pdf

Accesso riservato

Tipologia: Versione dell'autore revisionata e accettata per la pubblicazione
Dimensione 939.69 kB
Formato Adobe PDF
939.69 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1104751
Citazioni
  • ???jsp.display-item.citation.pmc??? 16
  • Scopus 27
  • ???jsp.display-item.citation.isi??? 25
social impact