Endothelial cells are critical elements in the evolution of all types
of cutaneous inflammation. They participate the pathological process t
hrough the synthesis and secretion of pro-inflammatory cytokines, incl
uding interleukin 1 (IL1), IL6, IL8, and the three colony stimulating
factors G-CSF, M-CSF, and GM-CSF and the two chemotactic factors gro-a
lpha and MCP. They also express a series of cell-surface proteins and
glycoproteins known as cell adhesion molecules that allow circulating
leukocytes to selectively bind to endothelial cells. In this paper we
discuss the role of endothelial cells in the evolution of cutaneous ne
crotizing vasculitis, an immunologically mediated clinical disorder as
sociated with segmental inflammation and fibrinoid necrosis of the der
mal venules, through the release of cytokines or their response to cyt
okines locally produced from leukocytes themselves primarily involved
in the endothelial cells injury. This interaction seems to involve and
modulate other biologically active systems including the fibrinolytic
system that can act amplifyng and self-perpetuating the tissue damage
through a non-immunologic mechanism.