It is possible that IL-17A may exerts a dual effect on fibrosis in the context of SSc, by acting in a different and often opposite way depending on its capacity to modulate the expression of various pro-fibrotic cytokines; interestingly in this study IL-17A production was significantly lower in SSc patients with PAH, leading to suppose that IL-17A could participate also in the modulation of physio-pathological processes involved in vascular disfunction. Here, IL17A is linked to pulmonary arterial hypertension.