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GPI — TNF
Text-mined interactions from Literome
Vijaykumar et al., J Biol Chem 2001
(Inflammation) :
These novel interactions are coupled to previously demonstrated PTK and PKC pathways, since the specific inhibitors of these kinases effectively blocked the
GPI induced
TNF-alpha production
Askari et al., Prostaglandins Other Lipid Mediat 2001
:
We, therefore, examined the
effects of
TNF-alpha on Ang II-induced increases in
PGI2 production in vascular smooth muscle cells ( VSMC )
Li et al., Acta Pharmacol Sin 2000
:
The responses of antisense IRAK-2 ODN to IL-1 and
TNF stimulated
PGI2 release are different
Kalsi et al., Mol Cell Biochem 2002
:
Therefore, we conclude that
TNF-alpha through activation of endogenous PLC
leads to cleavage of the
GPI-linkage of E5'N resulting in loss of E5'N from the extracellular surface
Nitto et al., Br J Pharmacol 2002
:
2
TNF-alpha induced the release of
GPI-80 from human neutrophils in a concentration- and time dependent manner ( in the range of 1-100 u ml(-1) and 30-120 min, respectively ), but did not affect surface GPI-80 levels ... 3 Cytochalasin B, genistein, and SB203580 but not PD98059 inhibited
TNF-alpha stimulated
GPI-80 release and neutrophil adherence at the same concentration ... In addition,
TNF-alpha induced
GPI-80 release was inhibited by blocking monoclonal antibodies specific to components of Mac-1 ( CD11b and CD18 ) ... 5 These findings indicate that
TNF-alpha stimulated
GPI-80 release from human neutrophils depends upon adherence via beta2 integrins
Itoh et al., Respirology 2003
:
TNF-alpha and MIF also
increased PGI2 production, but to a far lesser degree at high concentrations
Hazenbos et al., Blood 2004
(Inflammation) :
Strikingly, after stimulation with IgG-ICs,
tumor necrosis factor-alpha release, dendritic cell maturation, and antigen presentation were strongly
reduced by
GPI-anchor deficiency
Debierre-Grockiego et al., Infect Immun 2006
(Malaria, Falciparum) :
Here we show that Pfj is able to down-regulate
tumor necrosis factor alpha (TNF-alpha) production
induced by the
GPI of P. falciparum
Amaya et al., Pain 2009
(Disease Models, Animal...) :
The
PGI also induced a prominent
increase in IL-1beta and
TNF-alpha levels in the DRG and of cyclooxygenase-2 (COX-2) expression in neurons and satellite cells
Corradin et al., Eur J Immunol 1991
:
M
phi NO2- production in
response to rIFN-gamma and either exogenous
TNF-alpha or Leishmania was strongly enhanced by prostaglandin E2, consistent with such a mechanism
Conroy et al., PloS one 2009
(Inflammation...) :
Plasmodium falciparum
GPI ( pfGPI ) enhanced C5a receptor expression ( CD88 ) on monocytes, and the co-incubation of monocytes with C5a and pfGPI
resulted in the synergistic induction of cytokines ( IL-6,
TNF , IL-1beta, and IL-10 ), chemokines ( IL-8, MCP-1, MIP1alpha, MIP1beta ) and the anti-angiogenic factor sFlt-1 in a time and dose dependent manner
Newman et al., J Immunol 1991
(Mycobacterium avium-intracellulare Infection) :
The long term survival of peripheral blood derived human macrophages ( M phi ) from normal, healthy donors after infection with Mycobacterium avium intracellulare ( MAI ) correlates with the increased
induction of
TNF-alpha and IL-6 mRNA and protein by the infected M
phi
Brenneis et al., J Biol Chem 2011
(Disease Models, Animal...) :
Interestingly, we found that activation of E-prostanoid ( EP ) 2 and EP4 receptors, but not EP1, EP3,
PGI(2) receptor ( IP ), thromboxane A(2) receptor ( TP ), PGD(2) receptor ( DP ), and PGF ( 2 ) receptor ( FP ), efficiently
blocked LPS induced
tumor necrosis factor a (TNFa) synthesis and COX-2 and mPGES-1 induction as well as prostaglandin synthesis in spinal cultures
Bogdan et al., Eur J Immunol 1990
:
In the present study we investigated whether
TNF-alpha activates M
phi for killing of L. major parasites
Szabo et al., J Leukoc Biol 1990
:
The difference in the M
phi subset 's
TNF response remained even after the FcRI- M phi subset received a 2.5-fold increase in stimulation with the classical M phi induction regimen of IFN gamma plus bacterial cell wall product
Watari et al., Int J Cancer 2012
:
Low dose
AMF-26 effectively
inhibited the
tumor necrosis factor-a (TNF-a)- or the interleukin-1ß (IL-1ß) induced production of ICAM-1 in human umbilical vascular endothelial cells ( HUVECs )
Laplante et al., J Biol Chem 2011
:
In contrast, neither polymyxin B-treated nor delipidated ß ( 2 )
GPI stimulated
TNF-a production
Xie et al., Mol Immunol 2013
(Antiphospholipid Syndrome) :
Anti-ß ( 2 )
GPI/ß ( 2 ) GPI
induced TF and
TNF-a expression in monocytes involving both TLR4/MyD88 and TLR4/TRIF signaling pathways ... Overall, our results indicate that anti-ß ( 2 ) GPI/ß ( 2 )
GPI complex
induced TF and
TNF-a expression involving both TLR4/MyD88 and TLR4/TRIF signaling pathways and TLR4 and its adaptors might be molecular targets for therapy of antiphospholipid syndrome (APS)
Endo et al., Biochem Biophys Res Commun 1988
:
Both IL-1 and
TNF increased PGI2 production by EC in both a time- and dose dependent manner, and a combination of the two cytokines additively
enhanced PGI2 production
Kawakami et al., Biochem Biophys Res Commun 1986
:
The
stimulation of
PGI2 by
cachectin/TNF is comparable to that observed with interleukin-1, the monokine previously suggested to be the principal mediator of this effect ... The ability of
cachectin/TNF to
stimulate PGI2 production suggests that it may play a role in producing depressed blood pressure or shock
Hauser et al., Arch Surg 1995
(Wounds and Injuries) :
If so,
TNF-alpha down-regulation might
contribute to functional PM
phi suppression after systemic injury
Douvdevani et al., J Am Soc Nephrol 1995
:
It was found that clamping
pHi to values below 6.5
led to a markedly reduced
tumor necrosis factor-alpha production and phagocytosis
Orlinska et al., Immunopharmacology 1995
:
In the presence of 100 microM phloretin or DIDS the
pHi of activated monocyte was reduced to control value,
TNF-alpha production was
inhibited completely and total protein synthesis was inhibited by 61 % ... These data suggest that ( 1 )
TNF-alpha production, as other proteins, is
dependent on the
pHi of monocytes, and ( 2 ) TNF-alpha production, in contrast to total protein, is modulated by Na ( + ) -dependent HCO3-
Bradshaw et al., J Pharmacol Exp Ther 1995
:
Activation of murine bone marrow derived macrophages ( BMDM
phi ) with lipopolysaccharide (LPS)
causes rapid expression of
TNF-alpha , which as an autocrine factor enhances BMDM phi function through IL-1 beta and IL-6 production
Heise et al., J Virol 1995
(Cytomegalovirus Infections...) :
We conclude that ( i ) M phi activation is a prominent part of inflammatory responses to herpesvirus infection and ( ii ) IFN gamma and
TNF alpha play a critical role in both virus induced M
phi activation and control of herpesvirus growth independent of T and B cells
Pruimboom et al., Prostaglandins Leukot Essent Fatty Acids 1994
:
We conclude that LPS stimulation of hp-M
phi from liver disease
results in similar production of IL-1 beta, IL-6 and
TNF-alpha , but that the profile of the eicosanoid production of these M phi stimulated with LPS and A23187 differs from M phi of other origin and species
Alleva et al., Immunobiology 1993
(Neoplasms, Experimental) :
A PGE2-specific enzyme linked immunosorbent assay showed that TBH M phi T cell cultures contained significantly more PGE2 than those containing NH M
phi , and that exogenous
TNF-alpha increased PGE2 production in TBH M phi cultures more than in NH M phi cultures
Pomerantz et al., Biochemistry 1993
:
Indeed, cholesterol enrichment attenuated IL-1 beta-, PDGF-, and
TNF alpha induced
PGI2 synthesis relative to controls and was consistent with the results of in vitro labeling experiments demonstrating that cholesterol enrichment reduced the incorporation of [ 35S ] methionine into immunoprecipitable COX-1 and COX-2 following induction by PDGF
Nwariaku et al., Shock 1995
(Shock, Hemorrhagic) :
The purpose of this study was to determine if hemorrhagic shock alters the alveolar macrophage ( M
phi ) tumor necrosis factor (TNF) response to lipopolysaccharide (LPS) stimulation
Schofield et al., J Immunol 1996
:
The direct activation of endothelial cells by
GPI does not
require the participation of
TNF or IL-1
Moore et al., J Immunol 1996
(Lupus Nephritis) :
We hypothesized that
TNF-alpha enhanced the M
phi response to CSF-1 in MRL-lpr mice
Jungi et al., Immunol Lett 1996
:
Here we show that human monocyte derived M
phi respond to LPS by
tumor necrosis factor-alpha release and procoagulant activity
upregulation by a similar dose response curve in the presence or absence of serum, suggesting that humoral factors such as LBP are relatively unimportant in the activation of M phi
Sasaki et al., Blood 1997
(Hematologic Neoplasms...) :
Phorbol 12-myristate 13-acetate ( PMA ), interleukin-1 (IL-1), IL-3, IL-6, granulocyte-macrophage colony stimulating factor ( GM-CSF ), thrombopoietin (TPO), and
tumor necrosis factor-alpha (TNF-alpha) enhanced
PGI2-R mRNA expression
Wen et al., Cell Biol Int 1997
:
LPS, IL-1 beta and
TNF alpha effectively
enhanced BK-stimulated production of
PGI2 by HPASMC, while IFN gamma had only a weak effect on BK-stimulated PGI2 production ... Bradykinin induced
enhancement of
PGI2 production by LPS, IL-1 beta and
TNF alpha might be involved in the regulation of pulmonary vascular tension and prevent a paradoxical thrombogenic effect in endotoxin- or cytokine mediated inflammation and acute lung injury
Chou et al., J Neuroimmunol 1998
(Arthritis...) :
Adrenergic
regulation of LPS stimulated
TNF production by M
phi isolated from rats with streptococcal-cell-wall ( SCW ) -induced arthritis has been examined