scholarly journals Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Activates Type I Interferon Signals in Lupus Nephritis

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Leixi Xue ◽  
Lei Liu ◽  
Jun Huang ◽  
Jian Wen ◽  
Ru Yang ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Lupus Nephritis ◽  
Tumor Necrosis ◽  
Renal Damage ◽  
Mononuclear Cells ◽  
Type I Interferon ◽  
Type I ◽  
Type I Ifn ◽  
Inducible Genes ◽  
Necrosis Factor

Type I interferon (IFN) plays a central role in pathogenesis of systemic lupus erythematosus (SLE); tumor necrosis factor-like weak inducer of apoptosis (TWEAK) has been associated with a pathogenic role in lupus nephritis (LN). Thus we investigated whether TWEAK could induce the activation of type I IFN pathway in LN. We examined this in patient-derived peripheral blood mononuclear cells (PBMCs) as well as MRL/lpr mice, a murine LN model. Relative to the control cohorts, MRL/lpr mice showed severe histological changes, high index levels of renal damage, and elevated expression of type I IFN-inducible genes. After shRNA suppression of TWEAK, we observed that renal damage was significantly attenuated and expression of type I IFN-inducible genes was reduced in MRL/lpr mice. In parallel, siRNA of TWEAK also significantly reduced the expression of type I IFN-inducible genes in PBMCs relative to control transfections. In PBMCs, TWEAK stimulation also led to expression of type I IFN-inducible genes. Our results illustrate a novel regulatory role of TWEAK, in which its activity positively regulates type I IFN pathway in LN based on preclinical models. Our findings suggest TWEAK could act as a critical target in preventing renal damage in patients with LN.

scholarly journals RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages

2008 ◽  
Vol 4 (7) ◽  
pp. e1000099 ◽  
Author(s):  
Fuan Wang ◽  
Xiujuan Gao ◽  
John W. Barrett ◽  
Qing Shao ◽  
Eric Bartee ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Type I Interferon ◽  
Myxoma Virus ◽  
Type I ◽  
Human Macrophages ◽  
Necrosis Factor

Plasma Level of IL-1β in Disseminated Intravascular Goagulation

1991 ◽  
Vol 65 (04) ◽  
pp. 364-368 ◽  
Author(s):  
Hideo Wada ◽  
Shigehisa Tamaki ◽  
Motoaki Tanigawa ◽  
Mikio Takagi ◽  
Yoshitaka Mori ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Plasma Level ◽  
Organ Failure ◽  
Tumor Necrosis ◽  
Mononuclear Cells ◽  
Solid Cancer ◽  
Normal Individuals ◽  
The Relationship ◽  
Necrosis Factor

SummaryThe plasma level of interleukin-1β (IL-1β) was determined in normal individuals, patients with disseminated intravascular coagulation (DIC), patients in the pre-DIC period (within 7 days before the onset of DIC), and non-DIC patients to examine the relationship between DIC and the plasma ILlp level. The plasma IL-1β level was 0-0.085 ng/ml in normal individuals, with little difference being seen according to related age. It was significantly higher in the DIC group (0.19 ± 0.19 ng/ml) than in the pre-DIC group (0.05 ± 0.08 ng/ml) or the non-DIC group (0.09 ± 0.01 ng/ml). The plasma IL-1β level was not markedly elevated in leukemia patients, even in the DIC group, but it was significantly increased in the DIC group of solid cancer patients and was generally elevated in patients with sepsis. It was markedly elevated to 0.39 ± 0.26 ng/ml in patients with organ failure. When mononuclear cells were incubated with lipopolysaccharide, it was found that IL-1β, tumor necrosis factor, and tissue factor (TF) were released into the medium, and there was an increase of TF release from endothelial cells incubated with this medium. These results suggest that the increase in IL-Iβ reflected the activation of monocytes and may be an important factor in DIC and its associated organ failure.

scholarly journals Tumor Necrosis Factor Alpha Inhibits Type I Collagen Synthesis through Repressive CCAAT/Enhancer-Binding Proteins

2000 ◽  
Vol 20 (3) ◽  
pp. 912-918 ◽  
Author(s):  
Patricia Greenwel ◽  
Shizuko Tanaka ◽  
Dmitri Penkov ◽  
Wen Zhang ◽  
Michelle Olive ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Type I Collagen ◽  
Type I ◽  
Necrosis Factor Alpha ◽  
Gene Coding ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Stimulation Of

ABSTRACT Extracellular matrix (ECM) formation and remodeling are critical processes for proper morphogenesis, organogenesis, and tissue repair. The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) inhibits ECM accumulation by stimulating the expression of matrix proteolytic enzymes and by downregulating the deposition of structural macromolecules such as type I collagen. Stimulation of ECM degradation has been linked to prolonged activation of jun gene expression by the cytokine. Here we demonstrate that TNF-α inhibits transcription of the gene coding for the α2 chain of type I collagen [α2(I) collagen] in cultured fibroblasts by stimulating the synthesis and binding of repressive CCAAT/enhancer proteins (C/EBPs) to a previously identified TNF-α-responsive element. This conclusion was based on the concomitant identification of C/EBPβ and C/EBPδ as TNF-α-induced factors by biochemical purification and expression library screening. It was further supported by the ability of the C/EBP-specific dominant-negative (DN) protein to block TNF-α inhibition of α2(I) collagen but not TNF-α stimulation of the MMP-13 protease. The DN protein also blocked TNF-α downregulation of the gene coding for the α1 chain of type I collagen. The study therefore implicates repressive C/EBPs in the TNF-α-induced signaling pathway that controls ECM formation and remodeling.

scholarly journals Tumor Necrosis Factor Receptor 1 Expression Is Upregulated in Dendritic Cells in Patients with Chronic HCV Who Respond to Therapy

2010 ◽  
Vol 2010 ◽  
pp. 1-10
Author(s):  
Raul Cubillas ◽  
Katherine Kintner ◽  
Frances Phillips ◽  
Nitin J. Karandikar ◽  
Dwain L. Thiele ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Mononuclear Cells ◽  
Tumor Necrosis Factor Receptor ◽  
Mrna Levels ◽  
Specific Subset ◽  
Significant Difference ◽  
Chronic Hcv ◽  
Necrosis Factor

The present studies assessed the level of tumor necrosis factor receptor (TNFR) expression in peripheral blood mononuclear cells (PBMCs) subsets from patients with chronic HCV undergoing interferon /ribavirin-based therapy (Ifn/R). Methods. TNFR family member mRNA expression was determined using quantitative real-time PCR assays (RTPCRs) in PBMC from 39 HCV+ patients and 21 control HCV patients. Further subset analysis of HCV + patients (untreated (U), sustained virological responders (SVR), and nonresponders (NR)/relapsers (Rel)) PBMC was performed via staining with anti-CD123, anti-CD33, anti-TNFR1 or via RTPCR for TNFR1 mRNA. Results. A similar level of TNFR1 mRNA in PBMC from untreated HCV+ genotype 1 patients and controls was noted. TNFR1 and TNFR2 mRNA levels in PBMC from HCV+ patients with SVR were statistically different than levels in HCV() patients. A significant difference was noted between the peak values of TNFR1 of the CD123+ PBMC isolated from SVR and the NR/Rel. Conclusion. Upregulation of TNFR1 expression, occurring in a specific subset of CD123+ dendritic cells, appeared in HCV+ patients with SVR.

Type I Pityriasis Rubra Pilaris: Upregulation of Tumor Necrosis Factor α and Response to Adalimumab Therapy

2010 ◽  
Vol 14 (4) ◽  
pp. 185-188 ◽  
Author(s):  
Yao-Hua Zhang ◽  
Youwen Zhou ◽  
Nigel Ball ◽  
Ming-Wan Su ◽  
Jin-Hua Xu ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Normal Skin ◽  
Unknown Etiology ◽  
Type I ◽  
Lesional Skin ◽  
Messenger Ribonucleic Acid ◽  
Pityriasis Rubra Pilaris ◽  
Adalimumab Therapy ◽  
Necrosis Factor

Background: Pityriasis rubra pilaris (PRP) has unknown etiology and is often refractory to conventional therapies. Objective: To document a PRP patient's response to adalimumab therapy and to highlight the potential role of tumor necrosis factor (TNF) in the development of PRP skin lesions. Methods: A patient received adalimumab therapy at standard dosing intervals. In addition, the messenger ribonucleic acid (mRNA) of TNF in the lesional and perilesional normal skin was quantified in two patients with PRP. Results: The patient responded to adalimumab therapy and achieved clinical remission by 4 months. There was a significant elevation of TNF mRNA in the lesional skin of PRP. Conclusion: TNF upregulation is detected in PRP lesional skin, consistent with the observed clinical efficacy of TNF blockade for the treatment of PRP.

scholarly journals Cannabinoid Reduces Inflammatory Cytokines, Tumor Necrosis Factor-α, and Type I Interferons in Dermatomyositis In Vitro

2017 ◽  
Vol 137 (11) ◽  
pp. 2445-2447 ◽  
Author(s):  
Elizabeth S. Robinson ◽  
Paul Alves ◽  
Muhammad M. Bashir ◽  
Majid Zeidi ◽  
Rui Feng ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Type I Interferons ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor
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