Giant cell arteritis (GCA) is a chronic inflammatory disease that affects large and medium-sized arteries. It is the most common vasculitis in Western countries in individuals older than 50 years of age [1]. Temporal artery biopsy (TAB) is still considered the gold standard for GCA diagnosis showing the presence of a transmural inflammatory immune infiltrate in the temporal arteries [2,3]. Indeed, the arteries of GCA patients are characterized by the loss of immune privilege with the presence of an immune infiltrate in the three layers of the blood vessels. CD4+ T cells and macrophages are the most abundant immune cell subgroups that characterize the infiltrate of arteries. The presence of the immune infiltrate modifies the artery microenvironment with the production of cytokines/chemokines leading to arterial remodeling and resulting in ischemic events [4,5]. The triggers and the exact sequence of events that lead to GCA are not yet well characterized. In this scenario, microRNAs could play an important role in the onset and progression of GCA.

MicroRNAs (miRNAs) are small, non-coding RNAs that inhibit gene expression at the post-transcriptional level by blocking translation and/or promoting mRNA degradation. One miRNA can inhibit the expression of more than one mRNA. Several miRNAs have been reported deregulated in TABs from patients with GCA, but their role is still unknown. We previously reported that miR-146a, −146b, −21, −150, −155, -299-5p were up-regulated in inflamed TABs from patients with GCA than TABs from control patients without GCA [6]. Overexpression of miR-146a, −146b, −21, −155 in inflamed TABs has been documented by other teams in independent cohorts of patients [7,8] ranking them as the most probably involved in GCA pathogenesis.

The aims of the present work were to deepen the link between inflammation and miRNA up-regulation in GCA and to identify the role of miR-146a and miR-146b.