Tumor Necrosis Factor (TNF)

Old, Lloyd J.

doi:10.1126/science.2413547

Cited by 1,429 publications

(510 citation statements)

References 20 publications

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“…TNF is a cytokine involved in inflammation that stimulates the acute phase reaction (Old et al, 1985). Dysregulation of TNF production has been implicated in a variety of human diseases, including Alzheimer's disease, cancer, major depression, and inflammatory bowel disease (IBD) (Wajant et al, 2003;Clark et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Golgi Phosphoprotein 2 Down-regulates the Th1 Response in Human Gastric Cancer Cells by Suppressing IL-12A

Tang¹,

Ji²,

Tang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Golgi phosphoprotein 2 (GOLPH2) is a very important biomarker in a variety of diseases. Its biological function is not clear, particularly in gastric cancer. To investigate the role of GOLPH2 in human gastric cancer, and determine its effect on the Th1 lymphocyte response, its expression and that of IL-12A were measured by real-time PCR and immunohistochemistry. The relationship between GOLPH2 and IL-12A was analysed statistically. The effect of GOLPH2 on the Th1 lymphocyte response was investigated with an in vitro co-culture system. The results showed that in human gastric cancer, the expression of GOLPH2 was significantly higher and the expression of IL-12A was lower than in normal gastric mucosal tissues, and the expression levels of GOLPH2 and IL-12A were negatively correlated. In addition, obvious down-regulation of the Th1 response was observed when lymphocytes were co-cultured with gastric cancer SGC7901 cells over-expressing GOLPH2. GOLPH2 down-regulated the expression of IL-12A, and inhibited the expression of TNF-α and IFN-γ. The results indicated that GOLPH2 down-regulates the Th1 response via suppression of IL-12A in human gastric cancer, and this might provide a target for the prevention and treatment.

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Section: Discussionmentioning

confidence: 99%

Golgi Phosphoprotein 2 Down-regulates the Th1 Response in Human Gastric Cancer Cells by Suppressing IL-12A

Tang¹,

Ji²,

Tang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…1 Although TNF was first recognised for its ability to induce haemorrhagic necrosis of certain tumours, 2 it also mediates a variety of other physiological responses, including differentiation, inflammation and proliferation as well as apoptotic and necrotic cell death. 3 TNF also produces the systemic effects of fever and cachexia.…”

Section: Introductionmentioning

confidence: 99%

Granulocyte macrophage-colony stimulating factor and interleukin-3 increase expression of type II tumour necrosis factor receptor, increasing susceptibility to tumour necrosis factor-induced apoptosis. Control of leukaemia cell life/death switching

Rae

MacEwan

2004

Cell Death Differ

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Tumour necrosis factor (TNF) induces apoptosis in a range of cell types via its two receptors, TNFR1 and TNFR2. Here, we demonstrate that proliferation and TNFR2 expression was increased in human leukaemic TF-1 cells by granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-3 (IL-3), with TNFR1 expression unaffected. Consequently, they switch from a proliferative to a TNF-induced apoptotic phenotype. Raised TNFR2 expression and susceptibility to TNF-induced apoptosis was not a general effect of proliferation as IL-1b and IFN-c both proliferated TF-1 cells with no effect on TNFR expression or apoptosis. Although raised TNFR2 expression correlated with the apoptotic phenotype, stimulation of apoptosis in GM-CSF-pretreated cells was mediated by TNFR1, with stimulation of TNFR2 alone insufficient to initiate cell death. However, TNFR2 did play a role in apoptotic and proliferative responses as they were blocked by the presence of an antagonistic TNFR2 antibody. Additionally, coincubation with cycloheximide blocked the mitotic effects of GM-CSF or IL-3, allowing only the apoptotic responses of TNF to persist. TNF life/death was also observed in K562, but not MOLT-4 and HL-60 human leukaemic cell types. These findings show a cooperative role of TNFR2 in the TNF life/death switching phenomenon.

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“…Thus, mouse and human TNFα share about 86% of the aminoacidic sequences [20]. It is likely, therefore, that the murine response to hrTNFα may generate antibodies to epitopes present in TNFα from other species.…”

Section: Discussionmentioning

confidence: 99%

An anti-human recombinant tumor necrosis factor alpha (TNF?) monoclonal antibody recognizes an epitope in feline TNF?

et al. 2003

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-It is likely that the murine response to human recombinant TNFα (hrTNFα) may generate antibodies (Ab) to epitopes present in TNFα from other species. Here, we demonstrate that F5 antihrTNFα monoclonal antibody (mAb) recognizes feline TNFα while E8 anti-hrTNFα mAb failed to do so. In order to demonstrate that E8 and F5 mAb recognize different epitopes in the hrTNFα molecule, a constant concentration of E8 and variable concentrations of F5 were incubated with solid phase bound hrTNFα. Binding of E8 and F5 to hrTNFα was determined with anti-µ and γ chain specific Ab. F5 bound equally to hrTNFα in the presence or absence of E8 and the same amount of E8 bound to hrTNFα, in spite of the presence of F5. When using the E8 and F5 mAb for capturing the TNFα from the equine, canine, feline and bovine species, in supernatants of an ex vivo lipopolysaccharide (LPS)-stimulated whole blood cell culture, we only detected the feline TNFα by F5 mAb (p = 0.001). By a cytotoxic assay on L929 fibroblasts, we indeed demonstrated the feline TNFα production after the LPS stimulus. In an inhibition assay, the human and feline cytokines competed for F5, although the inhibition of native human TNFα binding to F5 was significant but only about 20% (p = 0.001). In conclusion, most likely the F5 anti-hrTNFα mAb recognizes an epitope in feline TNFα. Its immunomodulatory potential in the feline model remains to be studied. monoclonal antibodies / tumor necrosis factor alpha / cross-reactivity

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Tumor Necrosis Factor (TNF)

Cited by 1,429 publications

References 20 publications

Golgi Phosphoprotein 2 Down-regulates the Th1 Response in Human Gastric Cancer Cells by Suppressing IL-12A

Golgi Phosphoprotein 2 Down-regulates the Th1 Response in Human Gastric Cancer Cells by Suppressing IL-12A

Granulocyte macrophage-colony stimulating factor and interleukin-3 increase expression of type II tumour necrosis factor receptor, increasing susceptibility to tumour necrosis factor-induced apoptosis. Control of leukaemia cell life/death switching

An anti-human recombinant tumor necrosis factor alpha (TNF?) monoclonal antibody recognizes an epitope in feline TNF?

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