IL23A and temporal arteritis: Strengthening this, Greigert et al identified a positive feedback loop by which myofibroblasts (CD90+, a-SMA+, MYH11+) located in the neointima of GCA-arteries, in response to IFN-γ and TNF-α, produce Th1/Th17 polarising cytokines (IL-12/IL-23) thereby sustaining T-cell polarisation.23 This suggests a mechanism by which stromal cells contribute to maintain the inflammatory process of vascular lesions, through interactions with immune cells.