The function in the pathophysiology of SSc remains controversial:1. This activation has been demonstrated to enhance the expression of TGF-β by fibroblasts, thereby playing a role in the overall fibrotic processes.2. On the contrary, TLR-3 activation induces fibroblasts to produce IFN-I, which diminishes their capacity to produce extracellular matrix components. This evidence concerns the gene TGFB1 and systemic sclerosis.