**11. Newer concepts in GCA pathogenesis: Immune and vascular aging**

According to the 1990 ACR criteria for the diagnosis of GCA, age above 50 is considered a major criterion for disease diagnosis. [46] Susceptibility of elder persons for GCA is considered to be the result of two separate degenerative processes.

Firstly, immunesenescence is characterized by the shrinkage of the naïve T-cell pool, loss of immune-regulation and impairment of innate immunity. [47] More specifically, alterations in innate immunity functions, such as impairment of DC trafficking and prolonged maintenance of TLR expression raise the possibility of uncontrolled inflammatory reactions in immunopri‐ viliged sites. Furthermore, the immune aging process results in an increase in basal cytokine production by macrophages, dendritic cells, endothelial cells and fibroblasts.

Secondly, biochemical modifications in vessel wall extracellular structures, such as the disorganization of the elastic fibers, render the vessel wall extremely compliant. Vascular smooth muscle cells decrease in number and function. The media becomes thinner and deposition of calcium is not unusual. Beyond the alterations observed in biomechanical parameters, the "old" artery seems to provide a distinct micro-environment that potentially increases the risk for the formation of a novel spectrum of neoantigens and the persistence of inflammatory reactions. [48]
