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TNF activates cell differentiation. 1000 / 1237
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"Although TNFalpha was undetectable in any coculture conditions, TNFalpha has been reported to increase preadipocyte proliferation and block differentiation, and consistent with these reports, we observed that 100 ng/ml TNFalpha increased preadipocyte proliferation and potently blocked differentiation (XREF_FIG)."
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"A large number of inflammatory cells, including T cells, B cells, macrophages and dendritic cells, accumulate in the affected synovium, and these inflammatory cells, together with fibroblast like synoviocytes, express various cytokines, such as tumor necrosis factor alpha (TNFalpha), IL-6 and receptor activator of NF-kappaB ligand (RANKL), which are known to induce differentiation and activation of osteoclasts."
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"Then, the cell viability, expression of IL-6, IL-1β, and TNF-α and ROS production were determined.The THP-1-derived macrophages were induced differentiation and maintained as described above; then, the culture medium was removed, and 100 µL of MTT solution (2 mg/mL) were added per well for 4 h to allow MTT uptake."
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"Using our previously developed TEM assay [XREF_BIBR], we found that the presence of Ang-II alone, TNF alone, or valsartan (an Ang-II type 1 (AT1) receptor blocker) alone during cell migration, did not increase the differentiation of human adherent PBMC into fibroblasts after their migration through HCMEC in response to MCP-1 (XREF_FIG; see also XREF_SUPPLEMENTARY)."
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"In addition, macrophages produce cytokines and growth factors, such as IL-1, IL-6, TNF-alpha, TGFalpha, PDGF, VEGF and EGF, that stimulate proliferation, migration or differentiation of fibroblasts, keratinocytes and endothelial cells, and ultimately stimulate ECM deposition, re-epithelialization and neovascularization."
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"Because integrin alpha 5 beta 1 modulated both monocyte adhesion to fibronectin and also TNFalpha induced endothelial differentiation on that substrate, we designed in vivo experiments to assess the effects of blocking alpha 5 beta 1 on myeloid to endothelial differentiation (i.e. generation of vascular leukocytes) in vivo."
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"IL-4 is considered to be involved in chronic inflammatory responses [XREF_BIBR] and is deeply involved in allergic airway inflammation, in regulation of lymphocyte differentiation of naive helper T-cells to Th2 cells [XREF_BIBR] as well as modulating the TNF mediated growth and differentiation of dendritic cells (DC) [XREF_BIBR, XREF_BIBR]."
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"These results confirm those obtained with leukemic cell lines, suggesting that TNF-alpha can induce differentiation of fresh AML blasts, mainly toward the monocytic lineage, and that induction of differentiation seems to be closely linked to down-regulation of c-myc mRNA expression over the first 24 hr rather than to attenuation of cellular proliferation per se."
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"The M1 phenotype is activated by IFN-γ, TNF-α, IL-1, IL-6, IL-12, IL-23, and LPS to produce an inflammatory response.37 On the other hand, cytokines IL-4 and IL-13 produce stimulation and differentiation of the M2 phenotype that promotes resolution of inflammation and wound healing."
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"This study showed that the osteogenic potential of autologous MSCs was adversely affected when these cells were transplanted into wild-type mice, while abundant bone formation was observed when the MSCs were transplanted into immunosuppressed mice.In addition, studies conducted by Feng et al. [32] and Xing et al. [33] demonstrated that the addition of IGF-1 and TNF-α stimulated the osteogenic differentiation potential of dental pulp stem cells through the mammalian target of rapamycin (mTOR) and the NF-κB signaling pathways, respectively."
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"Chen et al. [XREF_BIBR] have shown that the effects of TNF-alpha on myogenesis and muscle regeneration are concentration dependent : a low concentration of TNF-alpha (0.05 ng/mL) promoted the differentiation of cultured myoblasts while higher concentrations (0.5 and 5ng/mL) inhibited it."
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"However, combinations of IL-4 and TNF-alpha acted in synergy to inhibit cell proliferation and induce monocytic differentiation of JCS cells, as shown by increased expression of the macrophage differentiation antigens (F4/80, Mac-1), stimulation of phagocytic activity, induction of non specific esterase and NBT reducing activities, increased plastic adherence and morphological criteria."
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"Furthermore, stem cell factor (Pan et al., 2013), tumor necrosis factor-a (TNF-α) (Shi et al., 2017), interferon-γ (IFN-γ) (He et al., 2017b), and BMP (Kim et al., 2010) have also been reported to promote dental pulp regeneration by increasing odontogenic MSCs migration and differentiation."
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"Here, we determined thatCD46 +/+ mice produce large numbers of M1 type macrophages with enhanced surface expression of MHC II and production of pro inflammatory mediators such as IL-6, TNF, IL-12, and IL-1beta In the presence of M-CSF or GM-CSF, CD46 signaling enhances monocyte-macrophage differentiation."
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"In contrast, mouse TNFalpha failed to induce TNF-Rp55-deficient mice derived Lin-c-kit+ HPCs to generate DCs with characteristic morphology, immunophenotype, and accessory function for T cells under the same culture conditions, suggesting a crucial role of TNF-Rp55 in TNFalpha mediated DC differentiation from HPCs."
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"Tumor necrosis factor (TNF)-alpha was found to be required for myogenesis, as shown by impaired regeneration in TNF-alpha null animals [XREF_BIBR]; however, the concentration of TNF-alpha required to promote differentiation is apparently very low, and higher levels can have the opposite effect; for example, whereas 0.05 ng/ml of TNF-alpha stimulated myogenesis, 0.5 and 5 ng/ml caused inhibition [XREF_BIBR]."
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"The conjunct of RANKL and RANK recruits TNF receptor associated factors (TRAFs), typically TRAF6, which activates multiple downstream signaling pathways, mainly NF-kappaB, MAPKs, and AKT, and thereby initiates osteoclast differentiation and bone resorption by inducing transcription and expression of osteoclast specific genes, such as tartrate resistant acid phosphatase (TRAP), cathepsin K, matrix metalloproteinase 9 (MMP-9), and C-Src."
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"Collectively, the results in XREF_FIG and XREF_FIG indicate that C5a acts on macrophages in the joint and other tissues to provoke their production of IL-1, IL-6, TNF, and IL-23, and together with tissue TGF-beta, promotes the differentiation and expansion of self-reactive T cells into Th17 cells."
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"To explore the possibility that TNF stimulates keratinocyte differentiation at least in part by regulating 1,25-(OH) 2D production we examined the effect of TNF on both 1,25-(OH) 2D production and differentiation (transglutaminase activity, cornified envelope formation) at different stages of differentiation."
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"Adding TNF-alpha from the start [TNF (+) cultures] potentiated progenitor cell proliferation and promoted early differentiation of CD1a+ DC precursors without affecting differentiation of CD14+ cells, which comprise bipotent precursors of DC and macrophages, nor of CD15+ granulocytic cells."
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"Several mechanisms of action have been proposed to account for these effects : TNF directly inhibits osteoblast differentiation; TNF augments osteoclast formation by inducing stromal cells to increase expression of RANKL and macrophage colony stimulating factor (M-CSF) and decrease that of osteoprotegerin (OPG); and TNF serves to synergize with pathways downstream of RANK to directly increase osteoclast differentiation."
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"96 In contrast, Lam et al. 97 have shown that although TNFalpha alone fails to induce differentiation of murine osteoclast precursors, priming with RANKL (with a concentration that is insufficient to induce osteoclastogenesis by itself) dramatically enhances TNFalpha induced osteoclast differentiation."
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"Certain authors demonstrated that TNF-alpha, IL-1beta and IL-6 induced osteoclast differentiation directly, in a RANKL independent manner, whereas others showed that a permissive level of RANKL is necessary for TNF-alpha-induced osteoclastogenesis, thus concluding that TNF-alpha alone can not induce osteoclast formation."
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"The regulatory effect of YAP on MDSCs is reflected in two aspects: First, directly transcribing chemokine CXCL5 to promote the recruitment of MDSCs in prostate tumor cells (72); Second, promoting the expression of IL-6, CSF1-3, TNF-α, IL-3, CXCL1/2, and CCL2 to promote the recruitment and systematic differentiation of MDSCs in the Kras: p53-mutant PDAC model (71)."
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"In contrast, the highest dose of TNF-alpha had the opposite effect on MSCs; cell content remained fairly constant throughout the study (XREF_FIG), while mineralized matrix content increased monotonically (XREF_FIG; all three timepoints differ, p < 0.05), consistent with progression towards terminal osteogenic differentiation and with previous reports of human MSCs treated with human TNF-alpha in the absence of dexamethasone [XREF_BIBR, XREF_BIBR]."
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"Endogenous TNFalpha released in co-cultures of CD34+ and allogeneic T cells was then demonstrated to mediate the rapid differentiation of a subset of CD34+ cells into monocytic and dendritic cells, whereas co-transplantation of CD34+ and T cells into NOD and SCID mice resulted in increased differentiation of mature dendritic cells."
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"On one hand, vascular endothelial growth factor, granulocyte-colony stimulating factor, granulocyte-macrophage colony stimulating factor, IL-6, tumor necrosis factor (TNF)-alpha, and so forth promote the proliferation and differentiation of bone marrow stromal cells into MDSCs by activating nuclear factor kappa B (NF-kappaB) and Janus kinase and signal transducers and activators of transcription (JAK and STAT) signal pathway [XREF_BIBR - XREF_BIBR]."
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"TNF morning peak augments hematopoietic stem and progenitor cell differentiation and increases vascular permeability to replenish the blood, while the evening peak exerts opposite effects by driving the renewal of hematopoietic stem cells and diminishing the vascular permeability [106]."
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"Osteoclastic differentiation is also regulated by numerous factors : osteoprotegerin (OPG); RANK-L (receptor activator of nuclear factor kappa B ligand, a transmembrane protein related to tumour necrosis factor [TNF], the binding of which to its RANK receptor induces osteoclastic differentiation); and soluble TNF receptors."
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"These results indicate that proinflammatory cytokine TNFalpha can promote Th17 cell differentiation in active RA patients via enhancement of monocytes derived IL-6 and IL-1beta production, and the signalling pathway is probably through TNFRI and TNFRII which are both expressed on the surface of monocytes."
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"Th1 profile cytokines, such as IL-2, INF-gamma, and TNF-alpha, which promote differentiation of naive T lymphocytes and macrophages, as well as the cytokines -- TGF-beta, IL-17, and IL-23 -- and Treg lymphocytes are involved in the pathogenesis of the type I reaction or reverse reaction."
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"XREF_BIBR In turn, IL-23 sustains Th17 proliferation, hence primarily increasing levels of IL-17 and IL-22 produced by these activated Th17 cells (It has been suggested that Th0 differentiation into Th17 is originally initiated by IL-6 and TGF-beta, and then supported by IL-23 and TNF-alpha)."
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"The small, yet significant, increases in TNFalpha and the increased osteoblastic response in young adult HRLF rats are similar to findings from other studies showing that low doses of TNF-alpha can stimulate osteoblast proliferation and osteogenic differentiation [XREF_BIBR - XREF_BIBR]."
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"To test this hypothesis, dendritic cells (DC) were generated in vitro from isolated monocytes, and changes in content, localization, and secretion of CyC and cathepsins S, L, and H (CatS, -L, and -H, repsectively) were followed in response to interleukin-4, enabling monocyte differentiation, and to tumor necrosis factor alpha (TNF-alpha), enabling DC maturation."
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"However, our previous in vitro study demonstrated that preconditioning of murine BM-MSCs using TNFalpha alone or a combination TNFalpha and IFNgamma did not promote osteogenesis; however, a combination of TNFalpha and LPS enhanced osteogenic differentiation including ALP activity and matrix mineralization."
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"Evidence has been provided, in fact, that tumor necrosis-factor-alpha (TNF-alpha) (via the p55 TNF-R1), IL-1beta, CD40 ligand (CD40L), and bacterial lipopolysaccaride (LPS) can promote DC differentiation in vitro, resulting in irreversible structural and functional changes associated with a mature DC phenotype, including downregulation of antigen uptake and processing capacity."
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"XREF_BIBR, XREF_BIBR VEGFA, another autocrine signal, has been described to contribute to the immobilisation of progenitor cells and the maintenance of stem cells, XREF_BIBR, XREF_BIBR, XREF_BIBR while TNFalpha, a well-known proinflammatory cytokine, can promote osteogenic differentiation of mesenchymal stem cells."
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"The results demonstrated that RANKL or TNFalpha did not effectively induce osteoclast differentiation from osteoclast progenitor cells derived from these mice into mature multinucleated osteoclasts, although c-jun N-terminal kinase (JNK) and NF-kappaB activation was apparently observed in osteoclast progenitor cells."
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"In addition to RANKL, recent studies have demonstrated there are several TNF family molecules which promote osteoclast differentiation, including TNF XREF_BIBR, decoy receptor 3 (DcR3) XREF_BIBR, FasL XREF_BIBR and TRAIL XREF_BIBR; indicating that activated T cells and inflammatory response can remodel bone homeostasis via these effector molecules."
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"TNF liked ligand 1A (TL1A) is another TNF family cytokine that acts through its receptor, death receptor 3 (DR3), to promote the differentiation of Th9 cells via an IL-2-STAT5-dependent mechanism, but not the lL-4-STAT-6 signaling axis involved in OX40 induced Th9 cell differentiation."
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"TNF enhances OC activity by directly promoting OC differentiation of bone marrow macrophages exposed to permissive levels of RANK-ligand (RANKL), XREF_BIBR by stimulating RANKL expression by T and B lymphocytes, XREF_BIBR by promoting stromal RANKL production by osteoblasts (OB), and by enhancing RANK and IL-1 expression by myeloid OC precursors."
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"TNF-alpha is released by activated monocytes, macrophages and T lymphocytes and contributes to both innate and adaptive immune responses, regulating growth, differentiation, survival and physiological function of a variety of different cells and further production of other cytokines, inflammatory mediators and enzymes XREF_BIBR - XREF_BIBR."
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"Moreover, this study found that PADI4 may contribute to cancer development and progression by increasing the expression of CXCR2, KRT14 and TNF-alpha, which activate pro inflammatory processes, angiogenesis, cell migration, cell proliferation and cell differentiation in tumor tissues."
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"Pre-treatment of PN/CIMP + GSCs with TNFalpha strongly reduced the G2/M accumulation in response to IR (XREF_FIG) as well as the number of gamma-H2AX foci (XREF_SUPPLEMENTARY), and these effects were inhibited by pre-treatment with IkappaB-SR, indicating that TNFalpha promotes MES differentiation coupled with increased radio-resistance in an NF-kappaB-dependent manner."
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"TNFalpha is known to directly induce bone resorption by activating mature osteoclasts and stimulating the proliferation and differentiation of osteoclast precursors or indirectly by inducing the expression of osteoclastogenic factors in stromal cells or osteoblasts [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"TNF synergizes with IL-1beta to induce synovitis by induction of chemokines, cytokines, e.g. IL-6, and prostaglandins by various cells, causes cartilage destruction by triggering the production of metalloproteinases by synovial fibroblasts and causes bone resorption by increasing the differentiation of osteoclasts 79."
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"Despite activating similar signaling pathways as does RANKL, TNF does not effectively induce osteoclast differentiation in the absence of RANKL; mechanisms that regulate the direct osteoclastogenic properties of TNF to limit pathological bone resorption in inflammatory settings are mostly unknown."
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"TNF-α weakens BMP9-induced tooth or osteogenic differentiation in human periodontal ligament fibroblasts117 118 or rat tooth sac cells.119 Interestingly, DKK1 alone inhibits BMP9-induced osteogenic differentiation, while promoting it in combination with TNF-α, the mechanism of which remains to be further explored."
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"Although TNF-alpha, IFN-gamma, and IL-1beta have been shown to induce the differentiation of THP-1 cells and increase the production of other immune related proteins [XREF_BIBR], none of these factors alone or in combination had a regulatory effect on the expression of CD300B protein."
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"This effect of TNF-alpha was observed only for + dex precultured MSCs, and not in dexamethasone-naive MSCs, suggesting that TNF-alpha is not sufficient to trigger differentiation, but can support mineralized matrix deposition that would otherwise require the presence of dexamethasone."
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"On the other hand, we also investigated the multipotent differentiation ability of DPCs, and the results showed that TNF-alpha treatment enhanced odontogenic and adipogenic differentiation of DPCs, as determined by ALP activity as well as alizarin red staining and oil red O staining, respectively."
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"In this co-culture system, it is likely that osteoclast differentiation was upregulated by TNF-alpha by both direct and indirect effects, including induced stromal cell and osteoblast production of RANKL, as well as increased sensitivity of osteoclast precursors to RANKL stimulation."
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"Together with our findings that TNF activates RBP-J signaling, which in turn suppresses osteoclastogenesis, the results support the idea that TNF activates feedback inhibitory mechanisms that are not effectively engaged by RANKL, and this stronger feedback inhibition helps explain why TNF is a weaker inducer of osteoclast differentiation than RANKL."
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"As tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) contributed crucially to the activation of inducible NO synthase (iNOS) gene transcription and to the differentiation of macrophages, we tested their roles in the induction of iMacs differentiation from bone marrow hematopoietic progenitor cells (HPC) of uncompromised mice."
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"Long-term clinical application has found that, except for gastrointestinal reactions, the use of TGP has no serious adverse reactions.Tumor necrosis factor-alpha (TNF-α) is an inflammatory cytokine that mediates key roles in proliferation, differentiation, apoptosis, immune regulation, and inflammation induction (Wijbrandts et al., 2008)."
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"Alternative cytokines and signaling molecules such as IL-25, IL-1, TSLP, Jagged-2, calcitonin gene related peptide and the TNF family member OX40 ligand (OX40L) have been proposed to enhance Th9 differentiation and/or T-cell production of IL-9, while cyclooxygenase-2-derived prostaglandins, programmed cell death ligand 2, and 1,25-dihidroxyvitamin D 3 inhibit Th9 polarization."
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"Expression of IkappaBalpha SR, an inhibitor of NFkappaB, does not reverse the differentiation defective phenotype of Ras expressing cultures, but does induce differentiation in cultures treated with tumor necrosis factor (TNFalpha) or in cultures expressing the RelA and p65 subunit of NFkappaB."
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"Taken together, these recent studies provided deeper mechanistic understanding of the dynamics of synovial fibroblast subpopulations during pathogenesis of arthritis, paving the way to the discovery of mesenchymal cell-targeted therapeutics beyond anti-TNFs.Along with interleukin-6 (IL-6), TNF-α stimulates synovial fibroblasts to produce receptor activator of NF-κB ligand (RANKL) promoting osteoclasts’ differentiation and activation [33]."
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"This was supported by experiments in which the authors demonstrate that RANKL and TNF successfully induced osteoclastogenic differentiation of osteoclast progenitor cells derived from NF-kappaB p50 and p52 deficient mice which were reconstituted with c-Fos and NFATc1 [XREF_BIBR, XREF_BIBR]."
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"M1 macrophages differentiation is induced by interferon-gamma, lipopolysaccharides, tumour necrosis factor (TNFalpha) and granulocyte-monocyte colony stimulating factor and are phenotypically characterized by high levels of interleukin IL-12, IL-23, TNFalpha, IL-1, IL-6, granulocyte -- macrophage colony stimulating factor (GM-CSF), CXC ligand 10 (CXCL10), inducible nitric oxide synthase (iNOS), human leucocyte antigen (HLA)-DR, reactive oxygen and nitrogen intermediates."
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"GSE reduced the secretion of TNF-α, IL-1 β and IL-6 in bone marrow-derived macrophages stimulated by lipopolysaccharide (P<0.01), inhibited the secretion of TNF-α, IL-1 β, IL-6, IL-12, IL-17 and IFN-γ in spleen cells of EAE mice immunized for 9 days (P<0.05 or P<0.01), and reduced the differentiation of Th1 and Th17 mediated by CD3 and CD28 factors (P<0.01)."
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"Whereas individual neutralization of IFN-gamma, IL-6, TNF, IL-17 and IL-4 did not restore iTreg differentiation of wild type T cells upon high TCR stimulation, combined blockade of these cytokines almost abrogated the ability of high doses of anti-CD3 mAb to suppress Foxp3 induction (XREF_FIG)."
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"Treatment with SB431542 promoted basal HuSKMC differentiation by up to threefold and partially rescued the blocking of differentiation caused by IL-1alpha and TNF-alpha, analyzed by either FI or CK activity suggesting that TGF-beta and ALK signaling may play a role in the IL-1alpha and TNF-alpha-induced inhibition of HuSKMC differentiation."
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"Thus, we demonstrated that the PA stimulated increase in IL-18 production in the IBC-NST biopsy samples may inhibit or block MDTC-to-HDTC differentiation after exposure to PAs; this differentiation may be mediated by other cytokines (IL-6 and/or IL-1beta, IL-1Ra, TNF-alpha and GM-CSF)."
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"To determine if BRG1 generally associates with NF-kappaB under conditions that lead to its activation or the association occurs only under certain conditions, such as during Schwann cell differentiation, HEK 293 cells were treated with TNFalpha, which stimulates NF-kappaB binding."
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"We found that the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) increased the level of intracellular reactive oxygen species (ROS) and caused cell senescence and osteogenic differentiation of cartilage endplate stem cells (CESCs), while rapamycin induced autophagy protected CESCs from TNF-alpha-induced oxidative stress and cell senescence."
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"As mentioned above, TNF-alpha and IFN-gamma secreted by the NK cells synergistically augmented differentiation of cells resulting in an increase in MHC class I, CD54 and B7H1 and their resistance to NK cell mediated cytotoxicity and decrease in cytokine and chemokine secretion by the NK cells cultured with differentiated cells [XREF_BIBR]."
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"Furthermore, it was demonstrated that TNF-α could increase reactive oxygen species (ROS) production in cells and cause osteogenic differentiation and cellular senescence in cartilage endplate stem cells (CESCs); however, autophagy could protect CESCs from oxidative injuries elicited by TNF-α and senescence [29]."
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"Moreover, transcriptomic analysis in the acute stages following sonication revealed a transient upregulation in proinflammatory cytokines and chemokines including CCL2, CCL3, and Tnf that have been found to promote migration, proliferation, differentiation and survival of neural progenitor cells favoring neurogenesis 31."
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"A large number of inflammatory cells, including T cells, B cells, macrophages and dendritic cells, accumulate in the affected synovium, and these inflammatory cells, together with fibroblast like synoviocytes, express various cytokines, such as tumor necrosis factor alpha (TNFalpha), IL-6 and receptor activator of NF-kappaB ligand (RANKL), which are known to induce differentiation and activation of osteoclasts."
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"Tumor necrosis factor alpha (TNF-alpha)-induced osteoclast formation have been demonstrated to play an important role in the pathogenesis of estrogen deficiency mediated bone loss, but the exact mechanisms by which TNF-alpha enhanced osteoclast differentiation were not fully elucidated."
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"Culture in the presence of TNF-alpha induced some differentiation, but only treatment with PMA and ionomycin (with or without prior culture in GM-CSF and IL-4) induced morphological and phenotypic changes consistent with DC like maturation, and even these maximally differentiated KG-1 cells showed lower levels of surface marker expression, macromolecular endocytosis, and ability to stimulate in allogeneic MLR compared with in vitro monocyte derived DCs."
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"Statin treatment did not alter serum levels of GM-CSF, TNF-alpha, and VEGF, supporting the hypothesis that statin treatment stimulates the differentiation of endothelial precursor cells into EPCs, suggesting that statins directly enhance the EPC migration ability in patients with CAD."
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"Moreover, vitamin D might exert immunomodulatory effects by inhibiting the expression of IL-6, IL-8, TNF-alpha, and TNF-gamma, modulate dendritic cell maturation, differentiation, and activation as well as induce the inhibition of antigen presentation XREF_BIBR, thereby dampen the autoimmune pathway incriminated in the pathogenesis of vitiligo."
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"In conclusion, we have shown that a PMT induced activation of G proteins in primary osteocytes and in the osteocyte like cell line MLO-Y4 leads to an elevated production and secretion of the osteoclastogenic cytokines RANKL and TNF-alpha, which efficiently contributes in an indirect manner to the differentiation of osteoclasts."
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"The selective up-regulation of TNFalpha inducible transcripts in this biphenotypic population led us to formulate the hypothesis that TNFalpha promotes endothelial differentiation of myeloid cells in vitro, and more importantly, that it may constitute, at least in part, the in vivo tumor microenvironment signal (s) to promote myeloid to endothelial plasticity."
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"It was reported that more than 40% of patients with IBD have bone loss, which becomes the major complication affecting the quality of life and productivity XREF_BIBR XREF_BIBR Excessive osteoclast differentiation induced by bone marrow Th17 TNFalpha cells was recently identified to contribute to bone loss in IBD XREF_BIBR."
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"Complementary to this evidence, studies in mice (105) and in rabbits (106) demonstrate that the adipocyte-promoted myeloid expansion and IL1β production inhibit B lymphopoiesis.Also, tumor necrosis factor alpha (TNFα) has been shown to be upregulated in HSCs upon aging, promoting myeloid differentiation skewing, HSC survival, and changes in the immunomodulatory properties through the activation of a nuclear factor-κB (NF-κB)-dependent gene program (94)."
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"On the other hand, several studies have shown that TNF-alpha contributes to neuroprotection and tissue regeneration after stroke, status epilepticus, and inflammation by affecting the survival, differentiation, and proliferation of neural stem and progenitor cells XREF_BIBR - XREF_BIBR."
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"Whereas physiological levels of Tnf are transiently up-regulated during myoblast regenerative responses to injury and stimulate differentiation, sustained high levels of TNF are associated with chronic inflammatory diseases and especially with muscle pathology associated with impairment of differentiation and muscle wasting."
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"Costimulatory signals initiated by the interaction between the tumor necrosis factor (TNF) ligand and cognate TNF receptor (TNFR) superfamilies promote clonal expansion, differentiation, and survival of antigen primed CD4 + and CD8 + T cells and have a pivotal role in T-cell-mediated adaptive immunity and diseases."
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"TNF liked ligand 1A (TL1A) is another TNF family cytokine that acts through its receptor, death receptor 3 (DR3), to promote the differentiation of Th9 cells via an IL-2-STAT5-dependent mechanism, but not the lL-4-STAT-6 signaling axis involved in OX40 induced Th9 cell differentiation."
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"Tumor necrosis factor-alpha (TNF-alpha), a potent cytokine involved in the regulation of osteoclast activity, promotes bone resorption via a primary effect on osteoblasts; however, it remains unclear whether TNF-alpha can also directly induce the differentiation of osteoclast progenitors into mature osteoclasts."
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"In the literature, it has been demonstrated that TNF-alpha induces the osteogenic differentiation of ASCs through the activation of the NF-kappaB signaling pathway [XREF_BIBR]; furthermore, NF-kappaB increases the expression of the transcriptional co-activator with a PDZ binding motif (TAZ), which stimulates ASCs into differentiating into osteoblasts through the activation of RUNX-2 and the repression of PPAR-gamma transcription."
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"In addition, we found that TNF-alpha promoted the osteogenic differentiation of hMSCs, as demonstrated by an increase in alkaline phosphatase (ALP) activity, as well as an increase in the expression of bone morphogenetic protein 2 (BMP-2), runt related transcription factor 2 (Runx2) and Osterix."
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"Split anergized NK cells are key mediators of cell differentiation since they secrete significant levels of IFN-gamma and TNF-alpha, which we have previously shown to drive differentiation of healthy, as well as transformed stem cells, in the absence of NK cell mediated cytotoxicity."
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"This indicates that in this disease model two mechanisms are essentially involved in inflammatory bone destruction : (a) Neighboring stromal cells need to provide excess amounts of proinflammatory factors, such as TNF, which induce osteoclast differentiation from mononuclear precursors; and (b) Osteoclastogenesis must overcome CD44 mediated cell-matrix interactions, which prevent tissue remodeling and damage."
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"In this work, dexamethasone-naive MSCs did not exhibit any substantial mineralized matrix deposition (XREF_FIG), suggesting that TNF-alpha is not sufficient to trigger in vitro osteogenic differentiation of MSCs, but instead stimulates and supports progression of + dex precultured cells toward terminal differentiation."
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"Increases in alkaline phosphatase point to the mechanism behind these changes, indicating that TNFalpha stimulates early osteogenic differentiation of valve interstitial cells, as has been observed in vitro under TGF-beta stimulation [XREF_BIBR], that can be protected against by preservation of endothelial function and reductions in oxidative stress."
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"We described here that pentoxifylline (PTX), which is well known to counteract tumor necrosis factor alpha (TNF alpha)-mediated inflammatory responses, augmented TNF alpha induced neuroblastoma cell differentiation in conjunction with growth inhibition and cell-cycle arrest in G1 phase."
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"Once released , TNF-alpha and IL-1 act on different target cells to promote the proliferation , activation , differentiation , and survival of macrophages ( Witsell & Schook , 1992 ; Fahlman et al ., 1994 ; Conte et al ., 2006 ) and all these effects enhance proinflammatory responses during sepsis , we confirmed an increase in GM-CSF levels at 17 and 48 h in the LPS group , when compared to the CTL group ."
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"Gene expression of vWF, CD31, VE-cadherin, Flk-1, and Flt-1 was significantly attenuated by Etanercept in the cells by 31.0 +/-6.5%, 74.0 +/-6.2%, 79.2 +/-2.9%, 79.0 +/-2.8%, and 48.7 +/-7.6% (n = 3, p < 0.05), respectively (XREF_FIG), suggesting that TACE and TNF-alpha signaling mediate the endothelial differentiation of MSCs in direct co-culture condition."
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"To mediate this process, we hypothesized that NK cells will have to first receive signals which will allow them to undergo split anergy resulting in a decrease in their cytotoxic function and an increase in the production of cytokines primarily, IFN-gamma and TNF-alpha, to promote differentiation of the cells."
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"TNF is a clinically validated etiological factor in inflammatory-erosive arthritis and is known to synergize with RANKL and macrophage colony stimulating factor (M-CSF) to enhance the differentiation of osteoclast precursors (OCPs) into bone resorbing osteoclasts in inflamed joints [XREF_BIBR, XREF_BIBR]."
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"Consequently, AIEC triggers a strong proinflammatory response via a series of signaling pathways: AIEC strains proficiently evade clearance and replicate within phagocytic cells inducing the release of tumor necrosis factor-α (TNF-α) [17,18] and also cardinal proinflammatory polarizing cytokines which drive Th1/Th17 differentiation [19]."
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"These findings were supported later in vitro studies in which the combined subinhibitory concentrations of MIF, TNF-alpha and IFN-gamma acted synergistically to inhibit erythroid differentiation and hemoglobin production by antagonizing the pattern of mitogen activated protein (MAP) kinase phosphorylation that normally occurs during erythroid progenitor differentiation."
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"Because M1 macrophages secrete large amounts of TNFalpha and IL-1beta that contribute to the differentiation of T H 17 cells, they are also believed to be important drivers of chronic inflammatory and autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, atherosclerosis, pulmonary fibrosis, and Crohn 's disease [XREF_BIBR - XREF_BIBR] (see Section 3.3)."
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"Ligation of the TNF receptor family costimulatory molecule OX40 (CD134) with an agonist anti-OX40 monoclonal antibody (mAb) enhances antitumor immunity by augmenting T-cell differentiation as well as turning off the suppressive activity of the FoxP3 (+) CD4 (+) regulatory T cells (Treg)."
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"Tumor differentiation was largely mediated by both IFN-gamma and TNF-alpha secreted by activated NK cells, since the addition of the combination of anti-TNF-alpha and anti-IFN-gamma retained the OSCSCs, MP2 pancreatic XREF_BIBR and A549 lung cancer cells in a non differentiated stage as assessed by susceptibility to NK cell mediated lysis and decreased B7H1 and MHC class I expression."
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"In inflammatory response, epithelial cells are also important sources of leukotrienes for stimulating the recruitment of circulating leukocytes, generation of cytokines and ROS, increased TNF-alpha expression and induce activation, differentiation and proliferation of B cells, that are involved with immune response."
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"Polysaccharides activate effector cells, such as macrophages, T lymphocytes, B lymphocytes, cytotoxic T lymphocytes, and natural killer cells to express cytokines, such as TNF-alpha, IFN-c, and IL-1beta, cytokines invariably possess antiproliferative activity, cause apoptosis and differentiation in tumor cells, and also secrete products like reactive nitrogen, oxygen intermediates, and interleukins [XREF_BIBR]."
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"Our findings suggest that TNF-alpha, BAFF and APRIL, and BCMA might contribute to the pathogenesis of BD possibly through augmentation of both innate and adaptive immune responses as well as by collaborating with other inflammatory cytokines to promote the activation and differentiation of effecter immune cells involved in the pathogenesis of BD."
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"XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR Growth differentiation factor-15 expression is induced by TNF-alpha, interleukins, P53, Egr-1, and macrophage colony stimulating factor, XREF_BIBR, XREF_BIBR, XREF_BIBR XREF_BIBR - XREF_BIBR with the protein widely being considered a biomarker for various diseases."
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"To further characterize the extent of MES differentiation, we performed microarray analysis of GSCs treated with TNFalpha and found significant enrichment of genes involved in wound healing and vasculature development, as well as, the NF-kappaB cascade and regulation of cell death related genes (XREF_FIG), suggesting that in addition to the canonical NF-kappaB pathway, TNFalpha induces a parallel MES differentiation in GSCs, which was further confirmed by qRT-PCR (XREF_SUPPLEMENTARY)."
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"In vitro studies have shown that TNF-alpha, along with IL-1alpha and IL1-beta, causes vacuolation of matrix cells within the follicle bulb and a decrease in the size of the matrix, as well as disorganization of follicular melanocytes and abnormal differentiation and keratinization of the precortical cells and the inner root sheath [XREF_BIBR]."
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"Furthermore, G. frondosa components could increase the secretion of cytokines, which are signaling molecules, including interferons (IFN), interleukins (IL), tumor necrosis factors (TNF) and lymphokines with antiproliferative activity, causing apoptosis and differentiation in tumor cells, thus further increasing the efficiency of immune related cells."
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"However, since previous in vitro studies have shown that TNF-alpha alone does not efficiently induce osteoclast differentiation of bone marrow derived M-CSF-dependent macrophages (BMMs) as RANKL does, TNF-alpha has been regarded as a cytokine that synergistically potentiates osteoclast differentiation and function in the presence of other cytokines such as RANKL, IL-1 and TGF-beta in vitro."
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"Such molecules include members of the osteoprotegerin and receptor for activation of NF-kB ligand (RANKL)/RANK pathway, where RANKL is a tumor necrosis factor family member secreted by osteoblasts with a role to trigger the differentiation of mesenchymal stromal cells to osteoclasts and speed up the complementary bone degradation processes."
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"Among cytokines produced by pDCs are IFN-Type I cytokines promoting Th1 cell differentiation via STAT4 transcriptional factor pathway (reviewed in), IL-6 which promotes myelin antigen specific Th17- and Th1-responses in experimental autoimmune encephalomyelitis (EAE), and TNF-alpha which induces oligodendrocyte apoptosis and mediates neuronal injury."
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"TNFalpha mediates its inflammatory functions by inducing the production of various proinflammatory cytokines and chemokines, activation of leukocytes and lymphocytes, inducing vascular permeability, enhancing the expression of adhesion molecules in immune cells as well as in the vascular endothelium, and promoting inflammatory cell migration, proliferation and differentiation XREF_BIBR - XREF_BIBR, XREF_BIBR, XREF_BIBR."
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"However, this favorable induction of IFN-gamma by EJHE-WR within the tumor microenvironment was accompanied by TGF-beta1 induction, probably along with an inflammatory cytokine e.g. TNF-alpha [XREF_BIBR, XREF_BIBR] that is common in such microenvironment, may further supports Th17 differentiation and thus induce IL-17 production as well [XREF_BIBR]."
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"To clarify the signaling mechanism of human myeloid differentiation by hematopoietic growth factors and cytokines, we investigated the role of extracellular signal regulated kinase (ERK) during the differentiation of human monoblastic U937 cells stimulated by granulocyte-macrophage colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)."
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"We herein examined the potency of osteoclast differentiation and maturation induced by fivefold supernatants in the stimulated human PDL cells with a physiologically high concentration (10 ng/mL) of recombinant TNF-alpha to human peripheral blood monocytes and macrophages in the simultaneous presence of the receptor activator of nuclear factor kappa-B ligand."
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"Some researches reported that IL-2, IL-12, IL-1alpha, IL-1beta, IL-6, and TNF-alpha could induce acute phase reaction, stimulate the growth and differentiation of hematopoietic precursor cells, promote the proliferation of synovial fibroblasts, and cause joint damage [XREF_BIBR] in the pathogenesis of RA."
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"Furthermore, both TNF-alpha and IL-6 induce synovial cells to release tissue degrading matrix enzymes, particularly members of metalloproteinase, and TNF-alpha stimulates abnormally the differentiation and proliferation of osteoclasts, which are responsible for bone erosions [XREF_BIBR, XREF_BIBR] (XREF_FIG)."
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"These data collectively indicate that Def6 regulated endogenous IFN-beta production contributes to the control of osteoclast differentiation by RANKL or TNF-alpha and also indicate that Def6 suppresses c-Fos and NFATc1 and Blimp1 axis at least partially via regulating an endogenous IFN-beta mediated inhibitory loop during osteoclastogenesis."
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"At advanced stages of COVID-19, intense activation of the NLRP3 inflammasome and TLR2-MyD88-NF-kappaB mediated pathways most likely create a cytokine environment enriched in IL-1beta, IL-23, IL-6, and TNF, which would further elicit Th17 differentiation and GM-CSF production by gammadeltaT17, Th17, and CD8 T cells (XREF_FIG)."
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"We also found that the expression level of TNF-alpha in intestinal mucosa of broiler chickens without narasin was significantly increased, which may be due to the fact that the body is in the stage of inflammatory reaction, and TNF-alpha produced by monocytes and macrophages is increased to promote cell proliferation and differentiation and repair body injury."
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"XREF_BIBR - XREF_BIBR Receptor activator of nuclear factor-kappaB ligand, a cell membrane bound TNF superfamily member, binds to receptor activator of nuclear factor-kappaB (RANK) expressed on osteoclast precursors, which then leads to the fusion, differentiation, and maturation of osteoclast."
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"25 Mouse recombinant IL-6 (50ngml -1; eBioscience; Santa Clara, CA, USA), human recombinant TGF-beta1 (2ngml -1; eBioscience), mouse recombinant IL-1beta (2ngml -1; eBioscience), mouse recombinant TNFalpha (1ngml -1; eBioscience), anti-IFNgamma Ab (XMG1.2; 10mugml -1) and anti-IL4 Ab (11B11; 5mugml -1) were added to the culture medium to induce Th17 cell differentiation."
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"Various concentrations of 1,25-dihydroxyvitamin D3 (vit D3; 10 (-9)-10(-7) M) and recombinant human tumor necrosis factor alpha (rTNF-alpha; 60-960 U/ml) were used to induce growth inhibition and differentiation of the human promyelocytic leukemia cell line HL-60 based on growth kinetics, colony formation, morphological analysis, nonspecific esterase (NSE) activity, surface antigen expression, and cytokine release."
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"We have previously shown that non cytotoxic concentrations (600-1200 U/ml) of recombinant mouse tumour necrosis factor-alpha (TNF-alpha) can induce differentiation of a subclone (JCS) of the WEHI-3B myelomonocytic leukaemia cell line into mature cells with the characteristics of macrophages."
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"First thought that IL-23 was the inducing cytokine for Th17 cells, three groups simultaneously discovered that TGF-β and IL-6 induced Th17 differentiation (28–30), while IL-1β and tumor necrosis factor (TNF)-α can potentiate Th17 differentiation in presence of IL-6 and transforming growth factor beta TGF-β (31–33)."
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"These findings suggest that the pro inflammatory cytokine TNF-alpha stimulates osteogenic differentiation of MSCs, an effect that can be blocked by the presence of anti-inflammatory agents like dexamethasone, with significant implications on the interplay between inflammation and tissue regeneration."
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"As TNF and IL-6 can induce osteoclast differentiation, the effect of BET inhibition on osteoclast differentiation is likely to result from a combination of direct and indirect mechanisms of action, the latter via inhibition of TNF and IL-6 production by cells in the synovial compartment 76."
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"Bacteria and their by-products can induce the release of pro inflammatory cytokines, such as macrophage chemoattractant protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha), interleukins (ILs) and prostaglandin E2, which directly or indirectly stimulate osteoclast differentiation."
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"The engagement of homotrimeric TNF-alpha to either receptor can activate three major signaling pathways : an apoptotic cascade initiated via the TNF-alpha receptor associated death domain, a nuclear factor kappa B (NFkappaB) signaling pro survival pathway implemented via NFkappaB mediated gene transcriptional actions, and a JNK (c-Jun N-terminal kinase) cascade involved in cellular differentiation and proliferation that is generally pro apoptotic [XREF_BIBR]."