Human tumour necrosis factor: precursor structure, expression and homology to lymphotoxin

Pennica, Diane; Nedwin, Glenn E.; Hayflick, Joel S.; Seeburg, Peter H.; Derynck, Rik; Palladino, Michael A.; Kohr, William J.; Aggarwal, Bharat B.; Goeddel, David V.

doi:10.1038/312724a0

Cited by 1,613 publications

(628 citation statements)

References 45 publications

Supporting

Mentioning

586

Contrasting

Unclassified

Order By: Relevance

“…Despite considerable structural identity of 36°7o and homology of 52°7o of the amino acid sequence [21] and functional similarities [20,22] TNF alpha and LT are also known to differ in their capacity to induce certain cytokines [12][13][14]. Both polypeptides share a common receptor [23], although they probably interact in a different fashion with this receptor [24].…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of differential regulation of interleukin‐6 mRNA accumulation by tumor necrosis factor alpha and lymphotoxin during monocytic differentiation

et al. 1990

View full text Add to dashboard Cite

In the present report we compare the capacity of two related cytokines, tumor necrosis factor (TNF) alpha and lymphotoxin (LT), to modulate mRNA levels of interleukin-6 (IL-6) in cells representing different stages of monocytic differentiation including the human leukemia cell lines HL 60, U 937, THP-1, MonoMac l and peripheral blood monocytes. We show that the capacity of TNF alpha and LT to induce IL-6 mRNA accumulation increases as monocytic differentiation proceeds with TNF alpha being more potent than LT, suggesting that alternate pathways may be used by differentiating cells to control expression of IL-6. In contrast, in monocytes which constitutively synthesize IL-6 transcripts, TNF alpha and LT treatment had opposite effects on levels of IL-6 mRNA accumulation. In these cells TNF alpha enhanced steady state levels of IL-6 transcripts due to mRNA stabilization, whereas LT shortened IL-6 mRNA half-life, most likely due to induction of a RNA destabilizer since LT-mediated downregulation of levels of IL-6 mRNA in monocytes could be prevented by inhibition of protein synthesis. Neither TNF alpha nor LT altered IL-6 mRNA accumulation by interfering with preexisting transcription factors since both TNF alpha and LT required de novo protein synthesis to exert their effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanisms of differential regulation of interleukin‐6 mRNA accumulation by tumor necrosis factor alpha and lymphotoxin during monocytic differentiation

et al. 1990

View full text Add to dashboard Cite

show abstract

“…Probe DNAs for IFN-a, IFN-b and b-actin were prepared as described (Harada et al 1990). The probe for TNF-a was a 750 bp of EcoRI fragment from l42-4 (Pennica et al 1984). The specific activity of each probe was Ϸ5 × 10 8 c.p.m./mg.…”

Section: Rna Preparation and Northern Blot Analysismentioning

confidence: 99%

Regulation of IFN‐α/β genes: evidence for a dual function of the transcription factor complex ISGF3 in the production and action of IFN‐α/β

et al. 1996

View full text Add to dashboard Cite

“…11 Its proinflammatory and antitumor activity was first noticed more than 100 y ago, but the protein was only identified in 1975. 12 Its gene was cloned in 1984, 13 and it was mapped to the short arm of chromosome 6, 14 near the HLA-B focus in the MHC. TNF-a is mainly produced by the activated macrophages and monocytes, although DC, mast cells, neutrophils, keratinocytes, smooth muscle cells, intestinal paneth cells, tumor cells, and microglial cells might also produce and release TNF-a.…”

Section: Introductionmentioning

confidence: 99%

TNF-α protects dendritic cells from prostate cancer-induced apoptosis

Pirtskhalaishvili

Shurin

Esche

et al. 2001

Prostate Cancer Prostatic Dis

View full text Add to dashboard Cite

We have recently shown that human prostate cancer (PCa) cells induced apoptotic death of the most potent antigen-presenting cells, dendritic cells (DC), which are responsible for the induction of specific antitumor immune responses. Here we have evaluated the effect of murine PCa cells RM-1 on the survival of immature and tumor necrosis factor-a (TNF-a)-stimulated mature DC. PCa cells and DC were co-incubated for 24 -48 h and DC apoptosis was assessed by morphologic criteria, Annexin V assay, and TUNEL staining. We have shown that co-incubation of RM-1 cells with DC is accompanied by an increased level of DC apoptosis, which was mediated by decreased expression of anti-apoptotic protein Bcl-2. Stimulation of DC maturation by TNF-a resulted in increased resistance of DC to PCa-induced apoptosis. In TNF-a treated mature DC, but not in immature DC, the expression of Bcl-2 was not blocked after exposure to RM-1-derived factors. Thus, these data suggest that TNF-a-induced maturation of DC increases their resistance to PCa induced apoptosis. This is likely to be due to the stabilizing of the expression of anti-apoptotic protein Bcl-2. The difference in the sensitivity of mature and immature DC to PCa-induced cell death should be considered during the design of DC-based clinical trials for PCa patients. Prostate Cancer and Prostatic Diseases (2001) 4, 221-227.

show abstract

Human tumour necrosis factor: precursor structure, expression and homology to lymphotoxin

Cited by 1,613 publications

References 45 publications

Mechanisms of differential regulation of interleukin‐6 mRNA accumulation by tumor necrosis factor alpha and lymphotoxin during monocytic differentiation

Mechanisms of differential regulation of interleukin‐6 mRNA accumulation by tumor necrosis factor alpha and lymphotoxin during monocytic differentiation

Regulation of IFN‐α/β genes: evidence for a dual function of the transcription factor complex ISGF3 in the production and action of IFN‐α/β

TNF-α protects dendritic cells from prostate cancer-induced apoptosis

Contact Info

Product

Resources

About