Giant cell arteritis (GCA) is an inflammatory chronic disease occurring exclusively in elderly individuals. Until recently, the disease has been considered a unique disease resulting from the interaction in the walls of susceptible arteries, between an unknown infectious agents with local dendritic cells (DCs), activated CD4 T cells and effector macrophages. Recent evidence has shown that this view was too simplistic and has clarified many of the pathogenetic aspects of the disease. Many genetic studies recently published have identified different new genes, including cytokines, adhesion molecules and regulators of innate immunity, as crucial players in the development and progression of GCA. Recent evidence suggests that there is heterogeneity of histological lesions in GCA, that are correlated with different immunological Th9 and Th17 signature. The recent demonstration that Varicella-zoster virus (VZV) antigen is present in the 64% of GCA-negative TAs and in the 73% of GCA-positive TAs could represent an important point of arrival in the search for a causative agent in the pathogenesis of a metameric disease such as GCA. In this context, cytokines such as IL-32 and IL-33 that act as a danger signal following tissue damage and infection are over-expressed in GCA arteries. Artery tertiary lymphoid organs, present in up to 50% of GCA-positive arteries, could represent the sites were primary immune responses and T- and B-cell autoimmune responses against viral antigens are organized. The recently demonstrated disturbed distribution of B cells in GCA could be also relevant in the pathogenesis of the disease, possibly contributing to the enhanced IL-6 response. Altogether, these evidences may clarify many pathogenetic aspect of the disease, also suggesting complexity greater than first imagined.

New insights into the pathogenesis of giant cell arteritis / Ciccia, Francesco; Rizzo, Aroldo; Ferrante, Angelo; Guggino, Giuliana; Croci, Stefania; Cavazza, Alberto; Salvarani, Carlo; Triolo, Giovanni. - In: AUTOIMMUNITY REVIEWS. - ISSN 1873-0183. - 16:7(2017), pp. 675-683. [10.1016/j.autrev.2017.05.004]

New insights into the pathogenesis of giant cell arteritis

SALVARANI, CARLO;
2017

Abstract

Giant cell arteritis (GCA) is an inflammatory chronic disease occurring exclusively in elderly individuals. Until recently, the disease has been considered a unique disease resulting from the interaction in the walls of susceptible arteries, between an unknown infectious agents with local dendritic cells (DCs), activated CD4 T cells and effector macrophages. Recent evidence has shown that this view was too simplistic and has clarified many of the pathogenetic aspects of the disease. Many genetic studies recently published have identified different new genes, including cytokines, adhesion molecules and regulators of innate immunity, as crucial players in the development and progression of GCA. Recent evidence suggests that there is heterogeneity of histological lesions in GCA, that are correlated with different immunological Th9 and Th17 signature. The recent demonstration that Varicella-zoster virus (VZV) antigen is present in the 64% of GCA-negative TAs and in the 73% of GCA-positive TAs could represent an important point of arrival in the search for a causative agent in the pathogenesis of a metameric disease such as GCA. In this context, cytokines such as IL-32 and IL-33 that act as a danger signal following tissue damage and infection are over-expressed in GCA arteries. Artery tertiary lymphoid organs, present in up to 50% of GCA-positive arteries, could represent the sites were primary immune responses and T- and B-cell autoimmune responses against viral antigens are organized. The recently demonstrated disturbed distribution of B cells in GCA could be also relevant in the pathogenesis of the disease, possibly contributing to the enhanced IL-6 response. Altogether, these evidences may clarify many pathogenetic aspect of the disease, also suggesting complexity greater than first imagined.
2017
4-mag-2017
16
7
675
683
New insights into the pathogenesis of giant cell arteritis / Ciccia, Francesco; Rizzo, Aroldo; Ferrante, Angelo; Guggino, Giuliana; Croci, Stefania; Cavazza, Alberto; Salvarani, Carlo; Triolo, Giovanni. - In: AUTOIMMUNITY REVIEWS. - ISSN 1873-0183. - 16:7(2017), pp. 675-683. [10.1016/j.autrev.2017.05.004]
Ciccia, Francesco; Rizzo, Aroldo; Ferrante, Angelo; Guggino, Giuliana; Croci, Stefania; Cavazza, Alberto; Salvarani, Carlo; Triolo, Giovanni
File in questo prodotto:
File Dimensione Formato  
1-s2.0-S1568997217301246-main.pdf

Accesso riservato

Tipologia: Versione pubblicata dall'editore
Dimensione 1.09 MB
Formato Adobe PDF
1.09 MB 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/11380/1144715
Citazioni
  • ???jsp.display-item.citation.pmc??? 14
  • Scopus 46
  • ???jsp.display-item.citation.isi??? 45
social impact