Potential roles of CCL2/monocyte chemoattractant protein-1 in the pathogenesis of cutaneous sclerosis

Scleroderma is a connective tissue disease of unknown etiology characterized by the excessive deposition of extracellular matrix in the skin. Cellular infiltrates of certain immune cells and pro-inflammatory mediators are suggested to play a crucial role in cutaneous fibrosis, forming complicated networks between fibroblasts and immune cells and/or cell-cell communications. Tissue-selective trafficking of leukocytes is mediated by combinations of adhesion molecules and chemokines. Although chemokines and their receptors are considered to be mediators of inflammation and fibrosis in scleroderma, their pathophysiological role remains incompletely understood. Recent studies suggest that CCL2/monocyte chemoattractant protein-1 plays an important role in the fibrotic process, including liver fibrosis, pulmonary fibrosis, and scleroderma. This review summarizes recent findings of the potential roles of CCL2 in cutaneous sclerosis in experimental animal models of scleroderma as well as human scleroderma.