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IL6 — SELE
Text-mined interactions from Literome
Cockerill et al., Circulation 2001
(Acute Disease...) :
Elevation of plasma high-density lipoprotein concentration reduces
interleukin-1 induced expression of
E-selectin in an in vivo model of acute inflammation
Landis et al., Arthritis Rheum 2002
:
Human peripheral blood monocytes were differentiated for 1-7 days in vitro and examined with respect to 1 ) uptake of MSU crystals, 2 ) expression of macrophage, dendritic cell, and activation markers, 3 ) secretion of tumor necrosis factor alpha (TNFalpha), interleukin 1beta (IL-1beta),
IL-6 , and IL-10, 4 )
activation of endothelial
E-selectin expression, and 5 ) enhancement of secondary neutrophil recruitment by endothelial cells ... MSU crystals induced TNFalpha, IL-1beta, and
IL-6 ( but not IL-10 ) secretion in undifferentiated monocytes, which in turn
promoted endothelial cell
E-selectin expression and secondary neutrophil capture under shear flow
Leeuwenberg et al., J Immunol 1990
:
Neither IFN-beta nor
IL-6 had any effect on the expression of
ELAM-1
Leeuwenberg et al., Eur J Immunol 1991
(Leukemia, Myeloid) :
ELAM-1 expression can selectively be
induced on human umbilical vein endothelial cells ( HUVEC ) by tumor necrosis factor,
interleukin 1 and lipopolysaccharide
Smadja et al., Pediatr Cardiol 2010
(Heart Defects, Congenital...) :
The study investigated soluble markers of endothelial damage or
activation ( thrombomodulin, soluble endothelial protein C receptor, and soluble
E-selectin ), inflammation (
interleukin-6 ), and angiogenic cytokine levels [ vascular endothelial growth factor ( VEGF ) and placental growth factor (PlGF) ] in 26 patients with CHD, 16 with reversible PAH ( median age, 2 years ) and 10 with irreversible PAH ( median age, 9 years )
Lewis et al., Mol Cell Biol 1994
:
In addition, an essential role for cooperative interaction between the two NF-kappa B complexes is shown by the requirement for both NF-kappa B sites to mediate
E-selectin promoter
activation by
interleukin-1 and p50/p65 expression
Weston et al., Transpl Immunol 1995
(Kidney Failure, Chronic) :
E-Selectin is a 115-kDa cell surface glycoprotein transiently expressed on vascular endothelium in
response to
interleukin-1 and tumour necrosis factor-alpha with a peak in expression at four hours
Del Papa et al., Arthritis Rheum 1996
(Wegener Granulomatosis) :
We found that AECA IgG from WG patients do not display any significant cytotoxicity but are able to up-regulate the expression of
E-selectin , intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 and to
induce the secretion of IL-1 beta,
IL-6 , IL-8, and MCP-1
Lou et al., J Neuroimmunol 1997
:
TBP I completely abolished TNF induced
IL-6 production and
E-selectin induction , while it partially inhibited TNF induced IL-8 production and up-regulation of ICAM-1 and VCAM-1
Ray et al., Biochem J 1997
:
Induction of the
E-selectin promoter by
interleukin 1 and tumour necrosis factor alpha, and inhibition by glucocorticoids
Miller et al., J Leukoc Biol 1998
:
Utilizing neutralizing antibodies, we show that CD40L mediated tissue factor and thrombomodulin modulation, as well as
E-selectin and VCAM-1 upregulation, is
independent of tumor necrosis factor alpha,
interleukin-1alpha , or interleukin-1beta production
Friedrichs et al., Arterioscler Thromb Vasc Biol 1998
:
Inhibition of tumor necrosis factor-alpha- and
interleukin-1 induced endothelial
E-selectin expression by thiol modifying agents