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The recognition of IL-17 producing T cells (Th17) has opened novel pathways to explain several features of SSc.
Considering SSc, studies using specific inhibitors of individual cytokines inhibitors have been found to be partially effective at alleviating the persistent fibrotic phenotype of fibrotic fibroblasts; moreover, individual cytokines appear to be responsible for complementary, overlapping features of SSc fibroblasts [14] [17].
Clinical features of SSc patients.
Raynaud's phenomenon and the loss of capillaries are characteristic features of SSc [ 27].
Whether ischemic macrovascular disease and/or accelerated atherosclerosis also are features of SSc is unclear.
Utilization of animal models has been instrumental in delineating complex pathologic features of SSc.
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Correlation analysis of CCL18 concentrations in supernatants with clinical features of SSc-IgG donors revealed a negative correlation with the time since lung fibrosis onset.
In light of fibrosis being the cardinal feature of SSc, it is interesting to note that IL-17 has also been implicated in fibrosis of the basal membrane in asthma [25] and the control of inflammatory response after bleomycin-induce lung injury, a model often exploited to study pulmonary fibrosis [26].
Hypoxia is a characteristic feature of SSc [ 45].
Another, and as yet poorly accounted for, feature of SSc is its overlap with thyroid abnormalities.
Recent studies have also identified B-cell genetic signature as a hallmark feature of SSc skin.
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