Autoimmune mechanisms of scleroderma and a role of oxidative stress

Abstract

Scleroderma is a fibrotic condition characterized by immunological abnormalities, vascular injury and increased accumulation of extracellular matrix proteins in the skin. Although the etiology of scleroderma has not yet been fully elucidated, a growing body of evidence suggests that extracellular matrix overproduction by activated fibroblasts results from complex interactions among endothelial cells, lymphocytes, macrophages and fibroblasts via a number of mediators, such as cytokines, chemokines and growth factors. Recent investigations have further suggested that reactive oxygen species (ROS) are involved and play a role of autoimmunology in scleroderma. In this review, current findings on the autoimmune mechanisms in the pathophysiology of scleroderma are described.