Editing Giant cell arteritis (section)

==Mechanism==
The pathological mechanism is the result of an inflammatory cascade that is triggered by an as of yet undetermined cause resulting in [[dendritic cell]]s in the vessel wall recruiting T cells and [[macrophage]]s to form granulomatous infiltrates.<ref name=":0" /> These infiltrates erode the middle and inner layers of the arterial [[tunica media]] leading to conditions such as aneurysm and dissection.<ref name=":0" /> Activation of [[T helper 17 cell|T helper 17]] (Th17) cells involved with [[interleukin]] (IL) [[Interleukin 6|6]], [[Interleukin 17|IL-17]], [[Interleukin 21|IL-21]] and [[Interleukin 23|IL-23]] play a critical part; specifically, [[T helper 17 cell|Th17]] activation leads to further activation of Th17 through IL-6 in a continuous, cyclic fashion.<ref name=":0" /> This pathway is suppressed with [[glucocorticoid]]s,<ref>{{cite journal | vauthors = Weyand CM, Goronzy JJ | title = Clinical practice. Giant-cell arteritis and polymyalgia rheumatica | journal = The New England Journal of Medicine | volume = 371 | issue = 1 | pages = 50–57 | date = July 2014 | pmid = 24988557 | pmc = 4277693 | doi = 10.1056/NEJMcp1214825 | veditors = Solomon CG }}</ref> and more recently it has been found that [[IL-6 inhibitor]]s also play a suppressive role.<ref name=":0" />