TGFB1 and systemic sclerosis: A wealth of evidence suggests that, once activated, SSc dermal fibroblasts establish a self-activation system by autocrine transforming growth factor (TGF)-β stimulation at least partially via upregulating cell surface receptors for latent-form TGF-β, such as integrin αVβ3, integrin αVβ5, and thrombospondin-1 [2-6].