Abstract
Scleroderma is a fi brotic condition characterized
by immunological abnormalities, vascular injury
and increased accumulation of extracellular matrix
proteins in the skin. Although the etiology of scleroderma
has not been fully elucidated, a growing
body of evidence suggests that the overproduction
of extracellular matrix proteins by activated
fi broblasts results from an imbalance between
synthesis and degradation of connective tissues.
A number of mediators, cytokines, chemokines
and growth factors secreted by infl ammatory cells
and mesenchymal cells (fi broblasts and myofi broblasts)
play an important role in the fi brotic process
of scleroderma. In this article, we describe recent
advances concerning immunological aspects in
the pathogenesis of bleomycin-induced murine
scleroderma, laying stress on the involvement of
interleukin-13 (IL-13) and plasminogen activator
inhibitor-1 (PAI-1).
