Gene interactions and pathways from curated databases and text-mining

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IFNB1 — IL1A

Text-mined interactions from Literome

Colton et al., J Neuroimmunol 1992 : Interleukin-1 activity was decreased by treatment with IFN gamma for 24 h while IFN alpha/beta increased IL-1 activity at 48 h. Removal of serum from the treatment media prevented the action of IFN alpha/beta on IL-1 production
Liberati et al., J Interferon Res 1992 : Moreover, rHuIFN-beta and natural IFN-beta induced significant and similar increases in 2'-5 ' adenylates, human Mx protein, and neopterin levels, but neither modulated beta 2-microglobulin, IL-1 alpha or beta synthesis
Molnarfi et al., J Neuroimmunol 2004 : Here we compare modulatory effects of IFNbeta on the production of proinflammatory cytokines ( IL-1beta, IL-1alpha , TNF, and IL-6 ) and IL-1Ra in human monocytes stimulated by lipopolysaccharides (LPS) and isolated plasma membranes of stimulated T cells ( msHUT ), which are likely to reflect monocyte activation in acute and chronic inflammation, respectively ... However, in monocytes activated by msHUT, the expression of cell associated and intracellular IL-1alpha was inhibited by IFNbeta , correlating with the inhibition of IL-1alpha transcript
Zang et al., Mult Scler 2004 (Multiple Sclerosis, Chronic Progressive...) : The results revealed that IFN beta inhibited intracellular production of interleukin (IL)-1b ( P < 0.01 ) in both monocytes exposed to in vitro treatment of IFN beta and monocytes analysed ex vivo from MS patients treated with IFN beta
Hirotani et al., Biochem Biophys Res Commun 2005 : Regulation of lipopolysaccharide-inducible genes by MyD88 and Toll/IL-1 domain containing adaptor inducing IFN-beta
Souvannavong et al., J Leukoc Biol 1990 : Neither IFN-alpha/beta nor IFN-gamma, when used alone or in the presence of silica, could induce the release of IL-1 by C3H/HeJ macrophages
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)
Jin et al., Brain Res 2007 : Although IFN-beta enhanced the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta , and nitric oxide ( NO ) by activated microglia, these molecules did not directly induce neurotoxicity in cultured cortical neurons
Clement-Lacroix et al., Lymphokine Cytokine Res 1991 : This synergistic effect seems to be restricted to the mitogenic activity since IL-1 induced PGE2 release and interferon-beta 1 (IFN-beta 1) production by fibroblasts was inhibited in the presence of FGFs, which by themselves were unable to stimulate the production of IFN-beta 1 and the release of arachidonate metabolites from the fibroblasts even at high concentration
Rodrigue-Gervais et al., J Immunol 2010 (Hepatitis C, Chronic) : Herein we report that NS3 dependent suppression of Toll/IL-1 domain containing adapter inducing IFN-beta- and IFN-beta promoter stimulator-1- but not MyD88 coupled pathogen-recognition receptor induced synthesis of proinflammatory cytokines ( IL-12 and TNF-alpha ) from DCs by hepatitis C virus ( HCV ) is a distinctive feature of a subgroup of chronically infected patients
May et al., J Biol Chem 1988 : `` Uninduced '' human FS-4 fibroblasts as well as those induced with interleukin-1 alpha , tumor necrosis factor, or bacterial lipopolysaccharide secrete at least five forms of IFN-beta 2 of apparent molecular mass in the range from 23 to 30 kDa which can be resolved by polyacrylamide gel electrophoresis under denaturing and reducing conditions
Kohase et al., J Interferon Res 1988 : To elucidate the mechanism of this inhibition, we examined the effect of IL1 on the synthesis of interferon-beta (IFN-beta) , stimulated with polyinosinate.polycytidylate [ poly ( I ) .poly ( C ) ]
Heike et al., Mol Immunol 1994 : GM-CSF and IFN-beta genes were expressed in response to PMA/A23187, poly ( I ) : poly ( C ), IL-1 alpha , forskolin, or LPS stimulation in differentiated P19 cells, whereas IL-3 and IL-4 genes were not expressed
Liu et al., J Immunol 1998 : Our data demonstrate a novel suppressive effect of IFN-beta and IL-4 on IL-1 activity in human microglia, suggesting that IFN-beta, a therapeutic agent used for multiple sclerosis, could have wider applications in the treatment of other central nervous system disorders in which IL-1 activity has been implicated in the pathogenesis