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TNF activates cell differentiation. 1000 / 1886
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"Whereas TGFβ exposure had limited consequences on OC differentiation in both WT and Fanca cells and no effect on the number of scored OCs per field (Additional file 1: Fig. S3), TNFα exposure fully rescued osteoclastogenesis in Fanca cells without modifying the dynamics of the differentiation process of the WT cells (Fig. 4A)."
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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, 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]."
eidos
"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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"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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"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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"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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"Some researchers have found that during the remodeling stage of bone, inflammatory cells infiltrated around the fracture site, such as monocytes, macrophages, lymphocytes, neutrophils, produce inflammatory factors, such as interleukin (IL)-1β, IL-6, IL-17, tumor necrosis factorF-α (TNF-α), receptor activator of nuclear factor kappa-B ligand (RANKL), macrophage colony-stimulating factor (M-CSF), which induce the differentiation and maturation of osteoclasts and lead to excessive absorption of bone graft."
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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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"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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"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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"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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"Transient activation of PKC during TNF-a signaling has been described in several human leukemic cell lines [9], however, our result indicates that activation of PKC is rather counteracting for TNF-a-mediated rapid onset of PKC AND C-MYC DURING TNF-a SIGNALING501Downloaded by [University of Wisconsin - Madison] at 13:39 06 January 2018FIGURE 3 Effect of PMA on TNF-a mediated differentiation in HL-60 cells."
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"GSH contributes the increase of bone resorption due to the increase of osteoclast number.Endogenous GSH is involved in TNFa stimulated osteoclast differentiation of BMMs Since exogenous GSH promoted TNFa stimulated osteoclast differentiation, we expected endogenousGSH to be also involved in 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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"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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"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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"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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"We show that while inducing myeloid progenitor apoptosis, TNFalpha promotes HSC survival and myeloid differentiation by activating a strong and specific p65 and nuclear factor-kappaB (NF-kappaB)-dependent gene program that primarily prevents necroptosis rather than apoptosis, induces immunomodulatory functions and poises HSCs for myeloid cell production."
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"However, TNF still led to residual Treg induction in cocultures of Tnfrsf1b CD4 T cells and macrophages, suggesting that in the absence of TNFR2, TNF may stimulate Treg differentiation via TNFR1, even though TNFR1 expression is not significantly correlated with CD4 expression in human lung ADC."
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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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"This effect can cause a failure of neutrophil and fibroblast functions, because TNF-alpha in particular increases the proliferation and differentiation of fibroblasts and the formation of alpha-smooth muscle actin and the extracellular matrix via transforming TGF-beta; also, TNF-alpha and IL-6 are strongly implicated as promoters of fibrosis [18, 24, 25]."
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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]."
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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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"In order to evaluate the effect of Wnt3a on the differentiation process of TNFalpha stimulated keratinocytes, primary keratinocytes were treated with TNFalpha (2 ng/mL) with or without Wnt3a for 24 h. Total RNA was collected and mRNA levels of involucrin, keratin 1, loricrin, and keratin 10 were analyzed via real-time PCR."
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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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"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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"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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"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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"Receptor activator of nuclear factor-kappa B ligand (RANKL) is a member of the TNF ligand super family that binds to RANK receptors on osteoclast precursors to drive differentiation and activity (Graphical Abstract).94 Osteoprotegerin (OPG) is a soluble decoy receptor for RANKL and denosumab is an anti-RANKL inhibitor that inhibits osteoclastogenesis to promote bone accrual."
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"Many osteoclast-activating factors (IL-6, IL-1β, HGF and TNF-α) are released by the mutual interactions of tumour and bone marrow cells with a major involvement of RANKL, the decoy receptor OPG, and MIP-1α a.RANKL is a member of the TNF family that binds to RANK on osteoclast precursors and promotes the production and differentiation of osteoclasts."
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"In the present study, we showed that the combination of TNF and IL‐6, representative proinflammatory cytokines, induced the differentiation of TRAP‐positive multinucleated TNF and IL‐6–induced osteoclasts from human peripheral blood monocyte‐derived macrophages, and that these TNF and IL‐6–induced osteoclasts had the ability to absorb bone matrix."
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"Studies using human and rodent mesenchymal stem cells (MSCs) show that TNF contributes to osteogenic differentiation through the activation of NFkappaB, with downstream induction of bone morphogenic proteins (BMPs), osterix, RUNX2, osteocalcin (OCN), and alkaline phosphatase (AP)."
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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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"Among them, TNF-α can kill tumor cells or suppress their growth and enhance the phagocytosis, proliferation and differentiation of neutrophils; IL-1β can activate immune cells, assist in T-cell proliferation, participate in the production of antibodies and promote inflammation; IL-6 is the major factor that mediates inflammation, as it can activate immune cells to exert an immunoregulatory effect [27]."
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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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"In addition, studies have shown that TNF-α activates a nuclear factor-κB-dependent gene program to promote HSCs survival and differentiation (35), which provides a possible target for us to explore the senescence and apoptosis of HSCs and inhibit the NF-kB pathway that may inhibit liver fibrosis by inducing apoptosis of HSCs."
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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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"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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"Many studies have shown that TLR4 and LPS activated the MSC1 phenotype expressing pro-inflammatory mediators, while interferon-y (INF-y) and tumor necrosis factor α (TNF-α) activated TLR3 and promoted the differentiation towards MSC2 phenotype, which regulated peripheral immune cells (Naftali-Shani et al., 2017; Ferreira et al., 2018; Almeria et al., 2019; Ananthakrishnan et al., 2020)."
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"Many studies have shown that TLR4 and LPS activated the MSC1 phenotype expressing pro-inflammatory mediators, while interferon-y (INF-y) and tumor necrosis factor α (TNF-α) activated TLR3 and promoted the differentiation towards MSC2 phenotype, which regulated peripheral immune cells (Naftali-Shani et al., 2017; Ferreira et al., 2018; Almeria et al., 2019; Ananthakrishnan et al., 2020)."
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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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"In contrast, pro-inflammatory M1 macrophages express enzymes such as nitric oxide synthase and cytokines such as TNF-α, IL-6, and IL-12, which promote inflammation, influence VIC and VEC properties and osteogenic differentiation potential, attract monocytes to the valve, and further propagate the inflammation [51]."
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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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"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 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-α and transforming growth factor (TGF-1) can induce the
proliferation, differentiation, and collagen production of fibroblasts
and promote the destruction of the basement membrane and the migration
of fibroblasts by activating proteolytic enzymes, thus participating
in the pathogenesis of ILD."
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"In the current pathophysiological model of psoriasis, pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, activate myeloid dendritic cells, which subsequently release IL-12 and IL-23.24 IL-12 induces differentiation of type 1 helper T (Th1) cells, which secrete pro-inflammatory cytokines TNF-α and IFN-γ, whereas IL-23 induces differentiation of type 17 helper T (Th17) cells, which secrete pro-inflammatory cytokines IL-17A, IL-17F, and IL-22."
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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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"However, if it is allowed to develop, it will become irreversible, thus leading to PI.Based on the results of subgroup analysis of TNF-α levels and data from relevant literature, low concentrations of TNF-α in the early stage after transplantation can indirectly promote the expression of osteoblast proteins such as osteocalcin, promote the differentiation and maturation of osteoblasts, and cause new bone formation."
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"Overall, the observed improvement in disease activity during pregnancy may be traced back to an increase in serum levels of (i) (in late pregnancy) interleukin (IL)-1 receptor antagonists (IL-1RA) and soluble tumour necrosis factor alpha (TNF-α) receptor (TNF-R), anti-inflammatory molecules neutralizing the effects of both IL-1 and TNF-α, respectively, and (ii) progesterone, which inhibits T helper (Th) 17 cell differentiation and promotes differentiation of Th2 and regulatory T (Treg) cells (Figure 1)."
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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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"IL-1β and TNF-α can promote the degradation of extracellular matrix, damage cartilage, promote the proliferation and differentiation of synovial fibroblasts, destroy articular cartilage and bone, and induce the production of inflammatory mediators, further aggravating the patient's condition."
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"The soluble TNF family member B lymphocyte stimulator (BLyS) is increased in serum of many lupus patients and promotes B cell survival and differentiation [XREF_BIBR], and interactions between co-stimulatory ligands and receptors on T and B cells, including CD80 and CD86 with CD28, inducible costimulator (ICOS) ligand with ICOS, and CD40 ligand with CD40, contribute to B cell differentiation to antibody producing plasma cells [XREF_BIBR]."
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"On the other hand, the GSH and NAC concentration (1-5 mM GSH and 1-4 mM NAC) in other reports and in our experiment showed that the stimulatory effects of GSH in RANKL induced osteoclast differentiation and TNFa stimulated osteoclast differentiation [34,35] are commonly used to scavenge ROS."
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"Moreover, testosterone deficiency causes an indirect deficiency of estradiol (159, 160), which leads to an enhanced bone loss through the increased production of several inflammatory cytokines (IL-1 and TNFα, IL-6), which stimulate osteoclastic differentiation and activity and promote osteoblastic apoptosis (161–165)."
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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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"93 In porcine intramuscular adipocytes, C1q/tumor necrosis factor-related protein 6 inhibited intramuscular adipocytes proliferation and promoted differentiation by the AdipoR1/MAPK signaling pathway94 and 1-deoxynojirimycin inhibited lipid accumulation by repressing of the ERK/PPARγ signaling pathway95 (Figure 3)."
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"Additionally, the data showed that PMT treated B cells are important to efficiently drive osteoclast differentiation from macrophages by secretion of inflammatory and osteogenic cytokines such as receptor activator nuclear factor kappa B ligand (RANKL), IL-1beta, IL-6 and TNF-alpha."
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"The granulocyte monocyte-colony stimulating factor (GM-CSF), vascular endothelial growth factor (VEGF), stem cell factor (SCF), prostaglandins, TNF-α, IFN-γ, and IL-18 were shown to promote the differentiation of functional MDSCs that contributed to the establishment of immunosuppressive niche and tumor progression (205–209)."
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"For example, our previous work has shown that TNF-alpha can act as a differentiation signal formurine myeloid leukemia WEHI-3B (JCS) cells and that its effects are greatly enhanced by IL-4.178 Apart from IL-4, TNF-alpha has been shown to interactwith other cytokines to induce leukemic cell differentiation."
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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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"In in vitro studies, SCFAs (especially butyrate) have been found to down-regulate the levels of TNF-α, IL-12 and IFN-γ by stimulating Foxp3(-) Treg cells, promote the differentiation of Tregs into Tr1 and Th3, and up-regulate IL- 4, IL-10 and TGF-β1 to suppress the immune response."
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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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"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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"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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"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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"To assess whether different forms of arthritis and disease activity could be distinguished by peripheral blood expression profiles of bone-regulatory factors including tumor necrosis factor (TNF)-superfamily [TNF related apoptosis inducing ligand (TRAIL), the Fas ligand (FasL), and the ligand for herpesvirus entry mediator (LIGHT)] and bone morphogenetic protein (BMP)-family members (BMP-2, BMP-4, BMP-6) as well as osteoblast differentiation gene Runx2."
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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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"In this early phase, this process is strictly controlled: the sympathetic nervous system, while inducing the differentiation of adaptive immunity cells toward a pro-inflammatory phenotype, by the production of pro-inflammatory TNF-α, IL-6, and IL-1β cytokines [7], also inhibits innate immune cells by the stimulation of β2- adrenergic receptors (β2-ARs)."
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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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"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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"For example, tumor necrosis factor-α (TNF-α) promotes the proliferation and differentiation of neural progenitor cells [62], while brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) can enhance the development and maintenance of neural circuits [63]."
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"As detected by IC95%, both in the cured and DTH individuals, the MultiGPGPG protein promoted the most increased differentiation of the single-producers into double- and triple-producers multifunctional CD4 T cells, which secret IL-2, TNF-α and IFN-γ, suggesting that MultiGPGPG induces stronger Th1 responses than MultiAAA (
Figures 9i–l
)."
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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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"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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"Among the slew of signaling cascades that takes place in an injured muscle microenvironment, interferon γ (IFN-γ) (Londhe and Davie 2011, 2013) and tumor necrosis factor (TNF) (Collins and Grounds 2001; Palacios et al. 2010; Jang et al. 2021) have been most well documented to directly regulate muscle progenitor cell proliferation and early differentiation."
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"There are two types of neurotrophin receptors: a nonenzymatic, trans-membrane protein of the tumor necrosis factor receptor (TNFR) family-p75 receptor and the tyrosine kinase receptors (TrkR) A, B, and C. Activation of the TrkBR by brain-derived neurotrophic factor (BDNF) or neurotrophin 4/5 (NT-4/5) promotes neuronal survival, differentiation, and synaptic function."
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"Finally, in one study in human iPSC-derived cerebral organoids, TNF-α decreased proliferation, increased gliogenesis and decreased neuronal differentiation through a reduction in fibroblast growth factor receptor 1 (FGFR1) signalling [90]Overall, these studies show that, similarly to glucocorticoids, the mechanisms elicited by cytokines to induce changes in proliferation and differentiation are vast."
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"However, we observed significantly increased differentiation bias towards myeloid lineage but decreased differentiation into B cell lineage of both TNFα-treated R878H and WT HSCs (Fig. 5H), indicating that TNFα promotes the differentiation bias to the myeloid lineage of both WT and R878H HSCs which is in line with the phenotype we observed in aged recipients.Now that R878H HSCs acquire survival advantage over WT HSCs upon TNFα insults, we wondered whether this effect can directly result in R878H-based clonal hematopoiesis."
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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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"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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"IL-4, IL-18, IFN-γ and TNF) that induced the differentiation of progenitor cells to cells of the secretory lineage such as GC and increased mucus production, thereby restoring the intestinal epithelial barrier.The crypt-villus morphology in the ileum provides the environment for digestion and absorption, while its structure could be simultaneously affected by commensal or pathogenic microorganisms residing in the gut."
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"The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/TNF receptor superfamily member fibroblast growth factor-inducible 14 (Fn14) pathway has been shown to play a critical role in the regulation of denervation-induced muscle atrophy as well as muscle proliferation, differentiation, and metabolism in adults."
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"Chitosan granules stimulate the immune response in various ways, such as by increasing the release of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, promoting the proliferation and differentiation of CD4+ and CD8+ T cells, stimulating humoral and cellular immunity, and inducing natural and acquired immune responses (22)."
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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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"Additionally, Wu et al. found that Lactobacillus reuteri treatment in TNF (Tumor necrosis factor)-induced intestinal inflammation led to a decrease in TNF production, repaired gut damage by activating the Wnt/β-catenin signaling pathway, and increased intestinal epithelial proliferation and differentiation, thereby strengthening the intestinal mucosal barrier against inflammation (32)."
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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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"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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"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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"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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"Lam J reported that although TNF-α alone cannot induce the differentiation of macrophages into osteoclasts, TNF-α and RANKL, which are nuclear factor kappa-B (NF-κB) receptor activator ligands, can significantly enhance the activity of NF-κB and stress-activated protein kinase/c-Jun N-terminal kinase."
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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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"It is noteworthy that there is a propensity to generate TH2-type cytokine responses because the secretion of TNFalpha, IFN-gamma, and IL-12, which promote the TH1 differentiation pathway of CD4+ and CD8+ into viral specific functional cells, is strikingly impaired by chronic alcohol."
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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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"Similar effects were observed in adipocytes in which RBP4 triggered TNF-α and IL-1β expression and release by activating the TLR4/myeloid differentiation factor (MD2) complex and TLR2 and the downstream toll/IL-1 receptor-domain-containing adapter-inducing interferon-β (TRIF) and myeloid differentiation primary response-88 and priming the nucleotide oligomerization domain-like receptor family pyrin domain containing-3 inflammasome."
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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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"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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"These results suggest that endogenous GSH of BMMs is involved in TNFa stimulated osteoclast differentiation in vitro.Effects of GSH on signal transduction related to osteoclast differentiationIn order to elucidate the mechanisms underlying GSHpromoted osteoclast differentiation, we examined the effects of GSH on well established signal transduction pathways of osteoclast differentiation."
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"Senescent AECIIs secrete high levels of interleukin, interferon, tumor necrosis factor, colony-stimulating factors, growth factors, and chemotactic cytokines, which promote fibroblast-to-myofibroblast differentiation and persistent tissue remodeling (Abbadie et al., 2017; Liu and Liu, 2020)."
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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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"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 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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"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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"On the basis of studies using several kinds of the arthritis mouse model, it has been shown that IL-17 plays a central role in the development of RA through activating synoviocytes, fibroblasts, endothelial cells, and macrophages to induce TNFalpha, which subsequently induces inflammation and osteoclast differentiation in multiple synovial joints [14,22]."
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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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"To reveal the gene expression responses in the cells prepared for MSC transdifferentiation and transplantation, the following treatments were applied: (I) IL-1β to suppress inflammation in adipose tissue, (II) TNF-α to promote cell proliferation and differentiation while suppressing apoptosis, (III) PolyI:C used for priming or boosting therapy to unleash lymphocytes and other factors of the targeted therapeutic pathway, (IV) LPS to boost the immune plasticity of the cells, and (V) IFN-γ to improve therapeutic effectiveness."
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"Since tumor necrosis factor alpha (TNF-alpha) and interleukin 1 (IL-1) induce osteoclast differentiation in certain settings, and since we observed both TNF-alpha and IL-1beta expression by monocytes transduced with IKKbeta SSEE (JO and YA, unpublished observations), we sought to determine whether these inflammatory factors were required for IKKbeta SSEE to induce osteoclast differentiation."
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"High lactate concentrations with low pH can decrease the production of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) by macrophages/monocytes.18 Moreover, studies have reported that lactic acid may inhibit the secretion of TNF by interfering with the glycolysis of human monocytes and suppress the differentiation of monocytes into dendritic cells, as well as the activation of T cells.19–22 For a more in-depth exploration of the immunomodulatory mechanisms of lactic acid, Peter K et al conducted a comprehensive analysis of its impact on gene expression during monocyte activation."
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"43 An iTRAQ proteomics study revealed that the TNF signaling pathway promoted the osteogenic differentiation of LF cells by activating Osx expression.12 Besides, numerous researches demonstrated that the TNF signaling enhanced the osteogenic differentiation ability of periodontal ligament stem cells (PDLSCs) in periodontitis.44–46 However, no studies were conducted to uncover the role of the toll-like receptor signaling pathway in OLF."
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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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"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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"Firstly, TNF-α promotes the differentiation of CD4 T helper (Th) cells 1796 so that the content of Th 17 cells in the bone marrow of OVX mice gradually increases.97 IL-17 secreted by Th17 cells upregulates RANK on osteoclast progenitors, increasing their sensitivity to RANKL stimulation.98 Furthermore, blocking IL-17 signaling prevented OVX-induced bone loss,99 suggesting that cytokines secreted by T cells play an important role in the pathological process of PMOP."
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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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"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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"TNF-α stimulates the differentiation of osteoclasts through nuclear factor kappa-B (NF-κB) and upregulates several target genes such as RANK and on the other hand suppresses differentiation of osteoblasts by inhibiting osteogenic factors such as runt-related transcription factor 2 (RUNX2) [47, 48]."
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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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"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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"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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"Haloperidol did not affect the release of proinflammatory cytokines IL-6, IL-8 or TNF-a in LPS stimulated macrophages.Effect of APDs on the production of potent Th1 and Th2 cytokine of human macrophagesThe cytokines IL-12 and IL-10 are prominent in Th1 and Th2 cell differentiation."
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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 addition, TNFα can induce anemia in patients with MM by directly inhibiting the formation and differentiation of red blood cells, reducing sensitivity to erythropoietin (EPO), and promoting IL-6 secretion by myeloma cells.IL1β is a pro-inflammatory cytokine11 that is primarily secreted by monocytes and macrophages and encoded by the IL1B gene."
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"Some essential factors associated with pyroptosis activator of nuclear factor-κB ligand (RANKL), macrophage colony-stimulating factor (M-CSF), TNF-α, and IL family, stimulate further differentiation and fusion of OCPs into multinucleated osteoclasts, leading to bone loss [64, 65] (Table 1)."
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"Interestingly, studies have also shown that the cocktail of TNF-alpha, IL-1beta, and IFN-gamma can direct the differentiation of pancreatic ductal cells towards the endocrine lineage and hence this may be important in the setting of regenerating the pancreas following its destruction in the setting of either diabetes or pancreatitis."
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"The random forests analyses, without and with adjustment for differences in demography, comorbidities and severity of disease, identified six biomarkers (adrenomedullin, TNF receptor-1, adipocyte fatty acid binding protein-4, TNF related apoptosis inducing ligand receptor 2, growth differentiation factor-15 and TNF receptor-2) to be strongly associated with CKD."
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"Osteoblasts and stromal cells control bone degradation by expressing the Macrophage-Colony Stimulating Factor (M-CSF) required for the proliferation of osteoclast precursors and the Receptor for Activation of NF-kB Ligand (RANKL), a TNF family member triggering their differentiation XREF_BIBR, XREF_BIBR - XREF_BIBR."