Regulatory mechanisms of collagen expression by interleukin-22 signaling in scleroderma fibroblasts

Systemic sclerosis (SSc) is an autoimmune disease characterized by irreversible and intractable tissue fibrosis of the skin and internal organs [1]. Previous findings indicate that inflammation, immune response and vascular damage lead to the activation of dermal fibroblasts, and then thickened dermis is resulted from uncontrolled excessive production of extracellular matrix (ECM) by the activated fibroblasts in the skin [2]. Although the mechanism of fibroblast activation in SSc is still unknown, many researchers have suggested that TGF-β1 may play a key role [3–5].