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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Immunol+Res
2015 ; 2015
(ä): 147616
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Endothelin Receptors Expressed by Immune Cells Are Involved in Modulation of
Inflammation and in Fibrosis: Relevance to the Pathogenesis of Systemic
Sclerosis
#MMPMID26090478
Elisa T
; Antonio P
; Giuseppe P
; Alessandro B
; Giuseppe A
; Federico C
; Marzia D
; Ruggero B
; Giacomo M
; Andrea O
; Daniela R
; Mariaelisa R
; Claudio L
J Immunol Res
2015[]; 2015
(ä): 147616
PMID26090478
show ga
Endothelin-1 (ET-1) plays a pivotal role in vasoconstriction, fibrosis, and
inflammation, the key features of systemic sclerosis (SSc). ET-1 receptors (ETA
and ET(B)) are expressed on endothelial cells, smooth muscle cells, and
fibroblasts, but their presence on immune cells has not been deeply investigated
so far. Endothelin receptors antagonists such as bosentan have beneficial effects
on vasoconstriction and fibrosis, but less is known about their potential
anti-inflammatory effects. We studied the expression of ET-1 receptors on immune
cells (T and B lymphocytes, monocytes, and neutrophils) and the link between ET-1
and inflammation in patients with SSc. We show here that ET-1 exerts a
proinflammatory effect in CD4+ T cells, since it induces an increased IFN-?
production; preincubation with antagonists of both receptors reduces IFN-?
production. Moreover, following ET-1 stimulation, neutrophils produce
proinflammatory mediators, thus amplifying the effects of activated CD4+ T cells.
Our data indicate that ET-1 system is involved in the pathogenesis of
inflammation and fibrosis typical of SSc, through the activation of T lymphocytes
and neutrophils and the consequent release of proinflammatory and profibrotic
cytokines. These findings suggest that dual ET-1 receptors antagonist therapy,
besides its effect on vasculopathy, has a profound impact on the immune system
favouring antiinflammatory and antifibrogenic effects.