Interferon β-1a Induces Tumor Necrosis Factor Receptor 1 but Decreases Tumor Necrosis Factor Receptor 2 Leukocyte mRNA Levels in Relapsing-Remitting Multiple Sclerosis

2009 ◽  
Vol 16 (3) ◽  
pp. 171-176 ◽  
Author(s):  
Reinhard Reuβ ◽  
Susanne Pohle ◽  
Kerstin Retzlaff ◽  
Jürgen Hemberger ◽  
Patrick Oschmann
Keyword(s):  
Multiple Sclerosis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Mrna Levels ◽  
Interferon Β ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis ◽  
Necrosis Factor

Tumor necrosis factor α and its receptors in relapsing-remitting multiple sclerosis

1997 ◽  
Vol 152 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Gianvito Martino ◽  
Antonella Consiglio ◽  
Diego M Franciotta ◽  
Angelo Corti ◽  
Massimo Filippi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Factor Α ◽  
Relapsing Remitting Multiple Sclerosis ◽  
Necrosis Factor

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.

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