The Potential Role of Cytokines in the Pathogenesis of Systemic Sclerosis (Scleroderma)

Abstract

Systemic sclerosis (scleroderma) is characterized by excessive fibroblastic activity taking place through mechanisms largely unknown. It has been speculated that soluble factors, collectively categorized as lymphokines or monokines, and released by inflammatory or other differentiated cells, may modulate fibroblast multiple functions including migration, chemotaxis and protein synthesis. Vascular endothelium itself, which is deeply injured in systemic sclerosis, is acting as a target for the action of cytokines and is an important producer of polypeptide mediators that contribute to the inflammatory reaction and to the establishment of fibrosis. Thus, interactions through soluble mediators between fibroblasts, endothelial cells and immunocompetent cells appear crucial for the development of systemic sclerosis lesions. The aim of the present study is to evaluate the available information on the role of cytokines and to discuss their potential influence in the pathogenesis of systemic sclerosis.