Soluble FAS serum levels are not associated with FAS-1377 G>A genotypes in vitiligo patients

摘要

Vitiligo is a sporadic skin disease marked by the loss of epidermal melanocytes and skin depigmentation. A combination of environmental, genetic, and immunologic factors is thought to play a role in its development [1,2]. FAS and FASLG are two members of the tumor necrosis factor family. They are important mediators of apoptotic signaling pathways [3]. FAS-induced apoptosis is an important homeostatic mechanism, particularly in organs with a high cellular turnover like the skin and cells of the immune system, which are thought to be involved in the autoimmune destruction of melanocytes [1,3]. FAS exists both as a trans-membrane receptor capable of signal transduction and as a secreted variant consisting only of the extracellular ligand-binding domain. This soluble form, sFAS, can be detected in the blood [4]. While not part of cellular signaling, circulating sFas can compete with its cellular counterpart for ligand binding, acting as a buffer for the signaling mechanism. This competitive inhibition can prevent apoptosis. It has been associated with autoimmune diseases [4, 5]. Studies of vitiligo in Chinese populations have identified elevated serum levels of sFas [6].