Gene interactions and pathways from curated databases and text-mining

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IL18 — TNF

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: IL18 → TNF (increases, TNF Translocation) Chandrasekar et al., Biochem Biophys Res Commun 2003*
    Evidence: Therefore, in the present study we investigated whether IL-18 expression is regulated by cytokines and oxidative stress in cardiomyocytes. TNF-alpha induced rapid and sustained activation of NF-kappaB whereas H(2)O(2) induced delayed and transient activation. Both TNF-alpha and H(2)O(2) induced IL-18 mRNA and precursor protein in cardiomyocytes, and IL-18 release into culture supernatants.
  • OpenBEL Selventa BEL large corpus: TNF → IL18 (increases)
    Evidence: IL-18 can act in synergy with IL-12 in regulating IFN-g (18). However, IL-18 also up-regulates other cytokines, such as TNF-a, IL-1b, and IL-8 in non-CD141 PBMCs, resting T cells, and NK cells (19). IL-18 up-regulates GM-CSF in PBMCs (20) and also in synovial membrane cultures, directly affecting macrophages to stimulate cytokine production (21).
  • OpenBEL Selventa BEL large corpus: TNF → IL18 (increases)
    Evidence: IL-18 is also ascribed many inflammatory functions that would be consistent with a role in angiogenesis. For instance, IL-18 stimulates the production of other proangiogenic cytokines, such as TNF-a, IL-1b and IL-8, from human PBMCs, the responding cells being predominantly resting T cells and NK cells. IL-18 stimulation of the chemokine IL-8 has also been shown in the macrophage cell line derived from histiocytic lymphoma cell, U937, and the myelomonocytic leukemia cell line, KG-1 (44, 45), to...
  • OpenBEL Selventa BEL large corpus: TNF → IL18 (increases)
    Evidence: Supportive of this function is the finding that IL-18 has been shown to stimulate production of angiogenic TNF-a (19).
  • OpenBEL Selventa BEL large corpus: TNF → IL18 (increases)
    Evidence: To determine the mechanism by which IL-18 mediates angiogenesis, we hypothesized that IL-18 may act through integrins present on HMVECs. TNF-a is angiogenic in part via its action on integrin avb3 (34). Thus, we examined whether blocking avb3 would inhibit IL-18-induced angiogenesis in the HMVEC migration assay. HMVECs were first incubated with anti-avb3 Ab or nonspecific control IgG at 25 mg/ml for 1 h before and during the chemotaxis assay. IL-18 (10 nM) was then used to stimulate HMVEC migrat...

Text-mined interactions from Literome

Sakao et al., Int Immunol 1999 (Shock, Septic) : Taken together, these findings demonstrate that IL-18 is responsible for the progression of endotoxin induced liver injury as well as down-regulation of endotoxin induced TNF-alpha production in P. acnes primed mice
Dinarello et al., Methods 1999 (Infection...) : IL-18 induces gene expression and synthesis of tumor necrosis factor (TNF) , IL-1, Fas ligand, and several chemokines
Gracie et al., J Clin Invest 1999 (Arthritis, Experimental...) : IL-18 independently promoted GM-CSF and nitric oxide production, and it induced significant TNF-alpha synthesis by CD14 ( + ) macrophages in synovial cultures ; the latter effect was potentiated by IL-12 or IL-15
De Caterina et al., Am J Clin Nutr 2000 (Arteriosclerosis) : Consumption of the n-3 fatty acid docosahexaenoic acid ( DHA ; 22 : 6n-3 ) reduced endothelial expression of vascular cell adhesion molecule 1 ( VCAM-1 ), E-selectin, intercellular adhesion molecule 1 ( ICAM-1 ), interleukin 6 (IL-6), and IL-8 in response to IL-1, IL-4, tumor necrosis factor , or bacterial endotoxin, with a half-maximal inhibitory concentration ( IC ( 50 ) ) of 1-25 micromol, ie, in the range of nutritionally achievable plasma concentrations
Kämpfer et al., Eur Cytokine Netw 2000 : Tumor necrosis factor-alpha (TNF-alpha) mediated a large decrease in IL-18 mRNA levels in the human keratinocyte cell line HaCaT, which was accompanied by a subsequent accumulation of IL-18 protein in the cell culture supernatants, which was shown to be biologically active
Ghigo et al., Infect Immun 2001 (Endocarditis, Bacterial...) : First, interleukin-10 suppressed C. burnetii stimulated production of TNF
Yoshida et al., Cell Immunol 2001 : IL-18 in the same concentration range stimulated the production of IL-12, TNF-alpha , and IFN-gamma in culture of PBMC ; however, IL-18 induced expression of ICAM-1 in monocytes was not inhibited by anti-IL-12, anti-TNF-alpha, or anti-IFN-gamma Ab, suggesting the independence of the upregulating effect of IL-18 on endogenous IL-12, TNF-alpha, and IFN-gamma production ... On the other hand, anti-ICAM-1 and anti-LFA-1 Abs inhibited IL-18 induced production of three cytokines, IL-12, IFN-gamma, and TNF-alpha , by 60 and 40 %, respectively
Wald et al., Eur J Immunol 2001 : Interleukin-18 (IL-18) , a pleiotropic cytokine produced by activated macrophages, plays significant roles in the immune response, inducing the secretion of IFN-gamma, TNF-alpha and IL-2, enhancing NK cell activity and potentiating the differentiation of Th1 cells
Takahashi et al., J Pharmacol Exp Ther 2002 : In the present study, we demonstrate that histamine inhibited the ICAM-1 expression in monocytes induced by IL-18 using flow cytometry and that the responses of IL-12, IFN-gamma, and TNF-alpha induced by IL-18 were concentration dependently inhibited by coexisting histamine, whereas IL-18 inhibited IL-10 production was reversed by the same concentrations of histamine
Veenstra et al., J Immunol 2002 (Neoplasms) : In contrast, IL-1alpha, IL-1beta, TNF-alpha , IFN-gamma-inducible protein-10, and Th2 cytokines such as IL-4 and IL-10 did not induce IL-18BPa
Yoshida et al., Life Sci 2002 (Disease Models, Animal...) : Interleukin-18 reduces expression of cardiac tumor necrosis factor-alpha and atrial natriuretic peptide in a murine model of viral myocarditis ... We examined the therapeutic effect of IL-18 on the modulation of TNF-alpha gene expression in failing heart in a murine model of heart failure caused by viral myocarditis
Huang et al., J Immunol 2002 (Pseudomonas Infections) : Because disease severity was increased in IFN-gamma ( -/- ) vs IL-18 neutralized mice, and since IL-18 also induces production of TNF , we tested for TNF-alpha in both groups
Splíchal et al., Vet Res 2002 (Salmonella Infections, Animal) : In the ileum, IFN-gamma, TNF-alpha , and IL-1beta were induced mainly by the virulent strain, whereas IL-18 was induced in highest quantity by non-virulent Salmonella
Werth et al., J Invest Dermatol 2003 : Although interleukin-12 is considered to act primarily on lymphocytes, provoking a shift from T helper 2 to T helper 1 cells and an increase in lymphocyte derived tumor necrosis factor alpha, we hypothesized that interleukin-12 might also affect tumor necrosis factor alpha secretion from skin cells ... Remarkably, the exogenous interleukin-12 totally blocked ultraviolet-B induced tumor necrosis factor alpha production ... Thus, interleukin-12 strongly inhibits tumor necrosis factor alpha production by noninflammatory skin cells, mostly or entirely through inhibition of gene transcription via an element within the first 1.2 kb of the tumor necrosis factor alpha promoter
Takahashi et al., J Pharmacol Exp Ther 2003 : In the same manner, salbutanol and terbutaline as well as norepinephrine, epinephrine, and isoproterenol regulated the IL-18 induced cytokine production, including IL-12, tumor necrosis factor-alpha or interferon-gamma through the stimulation of beta 2-AR. Together with the previous finding that ICAM-1/lymphocyte function associated antigen-1 interaction plays a crucial role in the IL-18 initiated cytokine network, the present study strongly suggested that the stimulation of beta 2-AR inhibited the IL-18 activated cytokine cascade through the inhibitory effect on ICAM-1 expression, contributing to finding a new method for clinical treatment
Lin et al., Crit Care Med 2003 (Hyperoxia) : Endogenous nitric oxide may be an important endogenous inhibitor of hyperoxia + tumor necrosis factor-alpha induced leukocyte recruitment and subsequently tumor necrosis factor-alpha, interleukin-1 beta, and GRO/CINC-1 release
Chandrasekar et al., Biochem Biophys Res Commun 2003 : TNF-alpha and H2O2 induce IL-18 and IL-18R beta expression in cardiomyocytes via NF-kappa B activation ... Both TNF-alpha and H ( 2 ) O ( 2 ) induced IL-18 mRNA and precursor protein in cardiomyocytes, and IL-18 release into culture supernatants
Jana et al., J Neurochem 2003 : Induction of tumor necrosis factor-alpha (TNF-alpha) by interleukin-12 p40 monomer and homodimer in microglia and macrophages
Maeda et al., J Invest Dermatol 2003 : Among T helper 1 cytokines, interleukin-4 mediated suppression of tumor necrosis factor-alpha was not affected by terfenadine, which, however, markedly restored mRNA expression of interferon-gamma or interleukin-2
Tada et al., Hokkaido Igaku Zasshi 1992 (Brain Neoplasms...) : TNF at a low dose ( 10 U/ml ) stimulated production of prostaglandin E2, Mn-superoxide dismutase, interleukin (IL)-6 and IL-8 by glioblastoma cells
Matsui et al., Expert Opin Ther Targets 2003 (Arthritis, Experimental...) : TNF-alpha , in turn, increases IL-18 expression in RA synovial cells
Dai et al., Arthritis Rheum 2004 (Arthritis, Rheumatoid) : IL-18 dose-dependently enhanced the production of IL-1beta and TNFalpha , but not IL-10, by monocytes following contact with RA synovial T cells or PHA prestimulated T cells
Schneider et al., J Immunol 2004 : IL-12 plus IL-18 rendered NK cells cytotoxic against Fas transfected target cells and promoted their production of IFN-gamma and TNF-alpha , which are both essential for sensitizing histamine producing cells to the Fas death pathway
Ichiyama et al., Inflamm Res 2004 : Moreover, the inhibitory effects of IVIG on IkappaBalpha degradation, interleukin-6 (IL-6) production, and E-selectin expression induced by TNF-alpha were evaluated by Western blot analysis, ELISA, and flow cytometry, respectively
Takahashi et al., Clin Immunol 2004 : Previously, we reported that tumor necrosis factor (TNF)-alpha production could be detected in human peripheral blood mononuclear cells ( PBMCs ) treated with relatively low concentration of LPS ( 1 ng/ml ), but that same concentration of LPS could not induce IL-18 production
Cheon et al., J Rheumatol 2004 (Arthritis, Rheumatoid...) : When RA FLS are stimulated with interleukin 1 or tumor necrosis factor-a , WISP3 mRNA is significantly increased
Desmet et al., Biochem Pharmacol 2005 : On the contrary, both RSG and TRO significantly potentiated TNF-alpha induced production of granulocyte/macrophage-colony stimulating factor, interleukin (IL)-6 and/or IL-8 in these cells
Striz et al., Immunol Lett 2005 : Tissue culture model of renal epithelial cells expressed IL-18 mRNA constitutively and released mature IL-18 in response to TNF-alpha and IFN-gamma
Stuyt et al., J Endotoxin Res 2005 (Acute-Phase Reaction...) : IL-18 is a pro-inflammatory cytokine of the IL-1 family and it induces IL-1, TNF , and IL-6, all of which are endogenous pyrogens
Krogh-Madsen et al., Am J Physiol Endocrinol Metab 2006 (Insulin Resistance) : We investigated the effects of TNF and IL-6 on IL-18 gene expression in skeletal muscle and adipose tissue ... TNF induced IL-18 gene expression in muscle tissue, but not in adipose tissue, whereas IL-6 infusion had no effect on IL-18 gene expression in either tissue
Krásná et al., Inflammation 2005 : Both cell lines upregulated IL-18R mRNA and IL-18R membrane expression in response to TNF alpha and other proinflammatory cytokines
Van Damme et al., J Invest Dermatol 1990 : This study focuses on interferon-beta (IFN-beta), interleukin-6 (IL-6), and interleukin-8 (IL-8) production by fibroblasts and epithelial cells in response to interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha)
Hodge et al., J Interferon Cytokine Res 2006 : The cumulative effects of IL-18 define a novel role for this cytokine as a molecular survival switch that functions to both decrease cell death through inhibition of the mitochondrial apoptotic pathway and enhance TNF induction of prosurvival factors
Yang et al., J Gastroenterol Hepatol 2007 (Reperfusion Injury...) : In contrast, IL-18 did not increase the TNF-alpha level and degree of lung injury, although it clearly enhanced the pulmonary MPO activity in normal animals
Takahashi et al., Br J Pharmacol 2007 : In the present study, we examined the effect of adenosine on the IL-18 induced up-regulation of ICAM-1 on human monocytes and production of IL-12, IFN-gamma and TNF-alpha by PBMC
Bastos et al., J Interferon Cytokine Res 2007 : Here, we investigated the role of IL-12/IL-18 on nitric oxide ( NO ) and tumor necrosis factor-alpha (TNF-alpha) production by CD11b ( + ) adherent peritoneal cells, focusing on the involvement of endogenously produced IFN-gamma
Choi et al., FEMS Immunol Med Microbiol 2007 (Candidiasis) : CpG oligodeoxynucleotides protect mice from lethal challenge with Candida albicans via a pathway involving tumor necrosis factor-alpha dependent interleukin-12 induction
Shembade et al., J Virol 2007 : Mouse fibroblasts lacking Ubc13 exhibit impaired Tax activation of NF-kappaB despite normal tumor necrosis factor- and interleukin-1 mediated NF-kappaB activation
Verri et al., Eur J Immunol 2007 (Arthritis, Rheumatoid) : OVA challenge induced the release of MIP-2, MIP-1alpha, TNF-alpha and LTB4 in the peritoneal cavity in an IL-15- and IL-18 dependent manner
Wang et al., Arthritis Rheum 2008 (Lupus Erythematosus, Cutaneous) : Keratinocytes from CLE patients expressed higher levels of IL-18 receptor on their cell surface in response to tumor necrosis factor alpha (TNFalpha) or interferon-gamma stimulation ... In response to IL-18 stimulation, these cells produced large amounts of TNFalpha
Inagaki et al., J Biol Chem 2008 : Tumor necrosis factor- and interleukin-1 induced activation of TAK1 was entirely normal in Tab1-deficient MEFs and could activate both mitogen activated protein kinases and NF-kappaB
Wittmann et al., Autoimmun Rev 2009 (Lupus Erythematosus, Cutaneous) : In CLE but not normal keratinocytes IL-18 strongly induces TNFalpha release, which then results in apoptosis
Silliman et al., Am J Physiol Cell Physiol 2010 : Tumor necrosis factor-alpha causes release of cytosolic interleukin-18 from human neutrophils ... In turn, TNF-alpha stimulation disrupted the association of IL-18 with F-actin, induced a FRET+ interaction of IL-18 with lipid rafts, and elicited IL-18 release ... We conclude that human PMNs contain IL-18 associated with F-actin in the cytoplasm and TNF-alpha stimulation causes dissociation of IL-18 from F-actin, association with lipid rafts, and extracellular release
Zhang et al., Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2010 : [ N-acetylcysteine antagonizes the Interleukin-18 induced expression of TNF-alpha and IL-6 in mouse vascular smooth muscle cells ] ... To explore the effect of N-acetylcysteine ( NAC ) on the interleukin(IL)18 induced expression of tumor necrosis factor (TNF) alpha and interleukin(IL) 6 in mouse vascular smooth muscle cells ( VSMC ) ... IL-18 significantly increased the mRNA expression and protein secretion of TNF-alpha and IL-6 ( P > 0.01 ) in a dose dependent and a time dependent ways ... NAC inhibited the mRNA expression and protein secretion of TNF-alpha and IL-6 induced by IL-18 ( P > 0.01 ) ... N-acetylcysteine antagonizes the production of TNF-alpha and IL-6 induced by IL-18 in VSMC
Bagchi et al., J Clin Immunol 2010 (Dysentery, Bacillary) : IL-18 promotes inflammation and induces IFN-gamma and tumor necrosis factor (TNF)-alpha as the expression of IFN-gamma and TNF-alpha cytokines was evident in this study
Marotte et al., Arthritis Rheum 2010 (Arthritis, Rheumatoid...) : Evaluation of signaling pathways suggested that TNFalpha induced IL-18 production through the ERK-1/2, protein kinase Cdelta (PKCdelta), and Src pathways, whereas IL-18BPa synthesis was mediated through the NFkappaB, PKC, Src, and JNK pathways
Tyagi et al., Mol Cell Endocrinol 2010 : In addition, like 17beta-estradiol, presence of medicarpin inhibited TNFalpha induced upregulation of interleukin-1 , and -6 mRNA levels in osteoblasts
Gutteberg et al., APMIS 1991 (Sepsis) : Using a whole blood in vitro model, we have investigated the effect of Escherichia coli ( E. coli ), Streptococcus agalactiae ( group B streptococci, GBS ) and tumor necrosis factor alpha (TNF) on the generation of lactoferrin (LF), interleukin-1 beta (IL-1) and tissue thromboplastin (TPL) in healthy newborns at term and their mothers
Elias et al., Chest 1990 (Pneumonia...) : To understand the processes regulating inflammation and fibrosis in the human lung, we characterized the effects of recombinant interleukin-1, tumor necrosis factor , and gamma interferon on fibroblast proliferation, collagen production, interleukin-1-alpha production, interleukin-1-beta production, and interleukin-6 production
Chan et al., Int J Oncol 1997 : Involvement of interleukin-1 in the differentiation inducing activity of tumor necrosis factor-alpha on a murine myeloid leukemia ( WEHI-3B JCS )
Carlo et al., J Pediatr 2011 (Cerebral Palsy...) : The analyses were focused on 5 cytokines ( interleukin [ IL] 1ß ; IL-8 ; tumor necrosis factor-a ; regulated upon activation, normal T-cell expressed, and secreted ( RANTES ) ; and IL-2 ) reported to be most predictive of CP in term and late preterm infants
Takeda et al., Int Immunopharmacol 2011 (Orthomyxoviridae Infections) : On day 2, tumor necrosis factor (TNF)-a production in BALF was also reduced significantly, but interferon-a, interleukin-12 , and interferon-? productions were augmented and natural killer ( NK ) cell activity was significantly elevated
Yamamoto et al., Rheumatol Int 2012 (Erythema...) : IL-18 induces IFN-?, IL-17, and TNF-a , which may play an important pathogenic role in AOSD
Ma et al., J Pharmacol Sci 2012 : We also demonstrated that pretreatment of cells with this compound prevented TNF-a induced expression of NF-?B target genes, such as interleukin 6, interleukin 8, monocyte chemotactic protein 1, cyclooxygenase-2 and inducible nitric oxide
Villacres et al., J Infect Dis 2012 (HIV Infections...) : Peripheral blood mononuclear cells ( PBMCs ) obtained at baseline were used to measure interleukin 1ß (IL-1ß), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 12 (IL-12), and tumor necrosis factor a (TNF-a) responses to Toll-like receptor (TLR) 3 and TLR4 stimulation
da Silva et al., Immunobiology 2013 : However, PGE2 alone stimulated the secretion of 208±89pgIL-10/ml whereas IL-18 alone did not stimulate the secretion of IL-10, IL-12, TNF-a or INF-?
Gunaydın et al., J Pediatr Surg 2012 (Acute Lung Injury...) : Aspiration of gastrointestinal decontamination agents produced histopathologic changes, elevated levels of malondialdehyde and surfactant protein D, reduced levels of antioxidant enzymes, and increased expression of inflammatory cytokines interleukin-1ß and tumor necrosis factor a. Curcumin treatments effectively attenuated the rats ' pulmonary inflammation responses ( as shown by reduced alveolar damage ), decreased serum malondialdehyde and surfactant protein D levels, and inhibited the expressions of tumor necrosis factor a and interleukin-1ß
Lin et al., Cytokine 2013 : Simvastatin treatment alone reduced constitutive Cx43 levels and prevented the TNF-a induced IL-18 up-regulation
Elias et al., Am J Respir Cell Mol Biol 1990 : We determined whether normal human lung fibroblasts expressed cell associated thymocyte stimulating activity in response to recombinant interleukin-1 ( rIL-1 ) ( alpha and beta ) and recombinant tumor necrosis factor ( rTNF )
Tsukamoto et al., Inflamm Bowel Dis 2013 : : Enzyme linked immunosorbent assay and AP assay showed interleukin-1ß induced TNF-a shedding in HCT116 and HT29 cells and TPA induced TNF-a release in U937 cells
Kitaura et al., Clin Dev Immunol 2013 (Arthritis, Rheumatoid...) : IL-12, IL-18, and IFN- ? induce apoptosis in bone marrow cells treated with TNF- a ??in vitro, and osteoclastogenesis is inhibited by the interactions of TNF- a -induced Fas and Fas ligand induced by IL-12, IL-18 , and IFN- ?
Gowen et al., Endocrinology 1990 : Human osteoblast cultures derived as out-growths from trabecular bone released tumor necrosis factor ( TNF alpha ) upon stimulation of the cells with human recombinant interleukin 1 ( IL1 ; 10 ( -13 ) -10 ( -11 ) M ), human recombinant granulocyte-macrophage colony stimulating factor ( 100-1000 U/ml ), and bacterial lipopolysaccharide ( 5-500 ng/ml )
Palladino et al., Ciba Found Symp 1987 (Neoplasms, Experimental) : Apart from their direct cytotoxic/cytostatic activities against tumours in vitro and in vivo, the in vivo antitumour activities of TNF-alpha or TNF-beta may involve the following biological activities : the induction of interleukin 1 production ; activation of polymorphonuclear neutrophil functions ; modulation of endothelial cell functions ; and augmentation of specific immune functions
Bachwich et al., Biochem Biophys Res Commun 1986 : Tumor necrosis factor stimulates interleukin-1 and prostaglandin E2 production in resting macrophages ... We have investigated the effect of tumor necrosis factor on the release of interleukin-1 and PGE2 from murine resident peritoneal macrophages ... Tumor necrosis factor causes an increase in the production of interleukin-1 and PGE2 with a maximum induction for both noted at 5.9 X 10 ( -8 ) M
Hoffman et al., Lymphokine Res 1986 : The effects of tumor necrosis factor on the production of interleukin-1 by macrophages
Le et al., J Immunol 1987 : Induction of membrane associated interleukin 1 by tumor necrosis factor in human fibroblasts
Männel et al., Rev Infect Dis 1987 : No TNF induced production of interleukin 1 ( which can induce similar effects ) was detected in macrophage/monocyte cultures
Libby et al., Am J Pathol 1986 : Endotoxin and tumor necrosis factor induce interleukin-1 gene expression in adult human vascular endothelial cells
Ferreira et al., Drugs 1993 (Hyperalgesia...) : The release of tumour necrosis factor-alpha (TNF-alpha) initiates the release of interleukin-1 and interleukin-8, which in turn liberate cyclo-oxygenase metabolites and sympathomimetic amines, respectively
Benveniste et al., Int J Dev Neurosci 1995 : In this study, we demonstrate that transforming growth factor-beta ( TGF-beta ), interleukin-10 (IL-10) and interleukin-6 (IL-6) inhibit tumor necrosis factor-alpha expression by primary rat astrocytes
Tsuji et al., Am J Pathol 1995 (Granuloma...) : Thus, interleukin-1 alpha and inducible nitric oxide synthase were induced mostly in the cells accumulated around the beads and also in some bronchiolar epithelial cells during the early phase ( 1 to 3 days ), whereas tumor necrosis factor-alpha was induced in the cells around the beads at the later resolution phase ( 3 to 7 days )
Aggarwal et al., Exp Cell Res 1995 : Diminished responsiveness of senescent normal human fibroblasts to TNF dependent proliferation and interleukin production is not due to its effect on the receptors or on the activation of a nuclear factor NF-kappa B
Judd et al., Am J Physiol 1995 : ZG cells released IL-6 and TNF , and this release was stimulated by lipopolysaccharide, interleukin-1 alpha, interleukin-1 beta, a protein kinase C activator, and a calcium ionophore without affecting intracellular adenosine 3 ', 5'-cyclic monophosphate ( cAMP ) content
Seatter et al., Arch Surg 1994 (Disease Models, Animal) : Tumor necrosis factor and interleukin-1 regulation by lipopolysaccharide pretreatment
Blasi et al., Infect Immun 1994 : Moreover, pretreatment of macrophages with recombinant TNF for 3 h enhances TNF and induces interleukin-1 production in response to both forms of Candida, while pretreatment for 18 h renders macrophages refractory to any stimuli
Becher et al., J Clin Invest 1996 : Soluble tumor necrosis factor receptor inhibits interleukin 12 production by stimulated human adult microglial cells in vitro
Yamamoto et al., Eur J Pharmacol 1996 (Disseminated Intravascular Coagulation) : Plasma interleukin-1 and TNF-alpha levels were elevated by lipopolysaccharide administration and the treatment with FR167653 ( 0.31 mg/kg/h for 4 h ) inhibited the increased plasma interleukin-1 ( 100.0 % ) and plasma TNF-alpha ( 89.2 % ) levels
Ortiz-Arduan et al., Am J Physiol 1996 (Endotoxemia) : Lipopolysaccharides (LPS), interleukin-1 beta, interferon-gamma (IFN-gamma), and TNF-alpha increase the levels of Fas mRNA in cultured mesangial and tubular cells
Klegeris et al., Brain Res 1997 (Alzheimer Disease) : First, it was shown that THP-1 cells could be induced to secrete significant amounts of TNF-alpha by interleukin-1 , lipopolysaccharide, interferon-gamma (IFN-gamma) and PMA alone or in combination with each other
Puren et al., J Clin Invest 1998 : IL-18 did not induce antiinflammatory cytokines, IL-1Ra, or IL-10, although IL-18 induction of TNFalpha was inhibited by IL-10 ... In the presence of IFNgamma, IL-18 induced TNFalpha was enhanced and there was an increase in the mature form of IL-1beta
Li et al., Eur J Pharmacol 1998 (Multiple Sclerosis) : Production of tumor necrosis factor-alpha and the lysosomal cysteine proteinase cathepsin B were markedly inhibited, but production of interleukin-1 increased
Bryson et al., Arch Biochem Biophys 1998 : It potently inhibited interleukin 1- and tumor necrosis factor stimulated proteoglycan release from both nasal and articular cartilage
Fiedler et al., Am J Respir Cell Mol Biol 1998 : The working hypothesis of the studies described herein was that inhibition of proteasome mediated IkappaB degradation would inhibit TNF-alpha induced nuclear factor-kappaB (NF-kappaB) activation, interleukin-8 (IL-8) gene transcription, and IL-8 protein release in A549 cells
Fulton et al., J Infect Dis 1998 : Regulation of interleukin-12 by interleukin-10, transforming growth factor-beta, tumor necrosis factor-alpha , and interferon-gamma in human monocytes infected with Mycobacterium tuberculosis H37Ra
Dinarello et al., J Allergy Clin Immunol 1999 : IL-18 induces gene expression and synthesis of TNF , IL-1, Fas ligand, and several chemokines