Systemic sclerosis (SSc) is a multisystem connective tissue disorder i
n which there is progressive fibrosis, Transforming growth factor beta
(TGF beta) has wide-ranging cellular actions, It is a potent chemoatt
ractant for human dermal fibroblasts, from which it may induce synthes
is of collagen, which suggests that it may have a central role to play
in the pathogenesis of SSc, This is supported to some extent by in vi
tro studies. SSc fibroblasts produce more collagens and fibronectin th
an normal fibroblasts and elevated TIMP levels have been observed, all
of which could be explained on the basis of TGF beta stimulation of f
ibroblasts, Some studies have suggested that fibroblasts are the sourc
e of TGF beta, However, the serum of patients with SSc is cytotoxic to
endothelial cells, which could culminate in TGF beta synthesis by the
m, with secondary fibroblast stimulation. The role of TGF beta remains
elusive, although it would seem an ideal candidate as a mediator of f
ibrosis in systemic sclerosis. (C) 1998 John Wiley & Sons, Ltd.