Gene interactions and pathways from curated databases and text-mining

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HNRNPF — IL6

Text-mined interactions from Literome

Manome et al., Immunology 1999 (Dermatitis, Contact) : Finally, we examined the effects of these chemicals on CD86 expression by three different macrophage subsets and DCs induced from the cultures of human peripheral blood monocytes in the presence of macrophage colony stimulating factor ( M-CSF ), M-CSF + interleukin-4 (IL-4), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and GM-CSF + IL-4, respectively
Nagayama et al., J Immunol 2000 : The ligation of DCs as well as Con A blasts by IL-12 induced the production of GM-CSF, IL-1beta, IL-6 , TNF-alpha, and IFN-gamma at the transcription levels
Liu et al., Chin J Cancer 2003 (Breast Neoplasms) : DCs were stimulated by granulocyte/macrophage colony stimulating factor ( GM-CSF ), interleukin-4(IL-4) , and tumor antigen
Kranzer et al., Infect Immun 2004 (Helicobacter Infections) : Stimulation of DCs with different concentrations of H. pylori for 8, 24, 48, and 72 h resulted in dose dependent interleukin-6 (IL-6) , IL-8, IL-10 and IL-12 production
Park et al., J Immunol 2004 : In addition, STAT3 phosphorylation in DCs was regulated by IL-6 in vivo, and STAT3 was necessary for the IL-6 suppression of bone marrow derived DC activation/maturation
Kitamura et al., Immunity 2005 : Here, we showed that IL-6-STAT3 signaling reduced intracellular MHCII alphabeta dimmer, Ii, and H2-DM levels in DCs ... Overexpression of cystatin C suppressed IL-6-STAT3 mediated increase of cathepsin S activity and reduction of MHCII alphabeta dimer, Ii, and H2-DM levels in DCs
Dillon et al., J Clin Invest 2006 (Inflammation) : Such DCs stimulate antigen-specific CD4+ T cells poorly due to IL-10 and the lack of IL-6
Hu et al., Infect Immun 2006 : In addition, Campylobacter infected DCs triggered activation of NF-kappaB and significantly stimulated production of interleukin-1beta (IL-1beta), IL-6 , IL-8, IL-10, IL-12, gamma interferon, and tumor necrosis factor alpha (TNF-alpha) compared to uninfected DCs
Hua et al., Nan Fang Yi Ke Da Xue Xue Bao 2006 : The DCs were derived from healthy human peripheral blood monocytes in the presence of granulocyte-macrophage colony stimulating factor, interleukin (IL)-4 and tumor necrosis factor (TNF) alpha
Gao et al., Toxicol Appl Pharmacol 2007 : After LPS stimulation, IL-6 , IL-10, IL-12 ( p70 ), and TNF-alpha levels significantly increased with both Pb-DCs and DCs, but Pb-DCs produced significantly less cytokines than did DCs, except for IL-10, which further supports Pb-DC preferential skewing toward type-2 immunity
Bharadwaj et al., Cancer Res 2007 (Pancreatic Neoplasms) : IL-6 was able to suppress DC differentiation and G-CSF mainly acted on the suppressing allostimulatory capacity of DCs
de Witte et al., Immunobiology 2007 : VLP interaction with DCs resulted in the up-regulation of co-stimulatory molecules and the production of the cytokines IL-6 , IL-8, IL-10 and IL-12p40
Xuan et al., Cell Physiol Biochem 2010 : High levels of IL-10 and IL-6 were observed in the presence of GA-treated DCs , whereas IFN-gamma and IL-12p70 production was similar with LPS- or GA-treated DCs
Chentoufi et al., Viral Immunol 2012 (Herpes Simplex) : Here we show for the first time that this is associated with LAT expression, since compared to LAT? virus : ( 1 ) LAT? virus interfered with expression of MHC class I and the co-stimulatory molecules CD80 and CD86 on the surface of DCs ; ( 2 ) LAT? virus impaired DC production of the proinflammatory cytokines IL-6 , IL-12, and TNF-a ; and ( 3 ) DCs infected in vitro with LAT? virus had significantly reduced the ability to stimulate HSV-specific CD8? T cells
Byun et al., Biochem Biophys Res Commun 2012 (Inflammation) : In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a, interleukin [ IL]-1ß, and IL-6 ) and activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38, c-Jun N-terminal kinase (JNK), and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Nieminen et al., PloS one 2013 : We found that IL-6- and IFN-a induced STAT3 phosphorylation and IFN-a induced STAT1 phosphorylation were impaired in plasmacytoid DCs ( pDCs ) from CD patients ( P?=?0.005, P?=?0.013, and P?=?0.006, respectively )
Khanna et al., Transplantation 1998 : In addition, however, a link was observed between the beneficial effect of donor BM and comparatively large numbers of donor major histocompatibility complex class II ( IAb+ ) -positive cells in recipients ' spleens, and in cultures of granulocyte-macrophage colony stimulating factor + interleukin-4 stimulated DCs from recipients ' BM