Pathogenic role of CCL2/MCP-1 in scleroderma

Abstract

Scleroderma is a connective tissue disease with unknown etiology characterized by excessive deposition of extracellular matrix in the skin. Cellular infiltrates of certain immune cells and proinflammatory mediators are suggested to play a crucial role in cutaneous fibrosis, forming complicated networks between fibroblasts and immune cells via cell-cell communications. Tissue-selective trafficking of leukocytes is mediated by combinations of adhesion molecules and chemokines. Recent studies have shown that an increase in proinflammatory chemokines has been associated with the initiation and/or development of fibrotic condition, suggesting that chemokines and their receptors may be important mediators of inflammation and fibrosis in scleroderma. In particular, CCL2/monocyte chemoattractant protein-1 (MCP-1) has been suggested to play an important role in scleroderma. This review will focus on the roles of CCL2 and its receptor during the process of cutaneous sclerosis, and also provide a current insight into the potential mechanisms of scleroderma.