scholarly journals TNF-α influences the lateral dynamics of TNF receptor I in living cells

2012 ◽  
Vol 1823 (10) ◽  
pp. 1984-1989 ◽  
Author(s):  
Meike Heidbreder ◽  
Christin Zander ◽  
Sebastian Malkusch ◽  
Darius Widera ◽  
Barbara Kaltschmidt ◽  
...  
Keyword(s):  
Living Cells ◽  
Tnf Receptor ◽  
Lateral Dynamics ◽  
Tnf Α ◽  
Tnf Receptor I

scholarly journals Lateral Dynamics of TNF Receptor I in Living Cells Studied with Single-Particle Tracking and Photoactivatable Fluorescent Probes

2012 ◽  
Vol 102 (3) ◽  
pp. 31a ◽  
Author(s):  
Meike Heidbreder ◽  
Christin Zander ◽  
Sebastian Malkusch ◽  
Darius Widera ◽  
Deepak Nair ◽  
...  
Keyword(s):  
Particle Tracking ◽  
Fluorescent Probes ◽  
Single Particle ◽  
Living Cells ◽  
Single Particle Tracking ◽  
Tnf Receptor ◽  
Lateral Dynamics ◽  
Tnf Receptor I

scholarly journals Development of a novel, nonimmunogenic, soluble human TNF receptor type I (sTNFR-I) construct in the baboon

2001 ◽  
Vol 91 (5) ◽  
pp. 2213-2223 ◽  
Author(s):  
Jason J. Rosenberg ◽  
Steven W. Martin ◽  
James E. Seely ◽  
Olaf Kinstler ◽  
Gregory C. Gaines ◽  
...  
Keyword(s):  
Polyethylene Glycol ◽  
Tumor Necrosis ◽  
Repeated Administration ◽  
Type I ◽  
Tnf Receptor ◽  
E Coli ◽  
Tnf Α ◽  
Covalently Linked ◽  
Tnf Receptor I ◽  
Necrosis Factor

Pharmacokinetics and immunogenicity of six different recombinant human soluble p55 tumor necrosis factor (TNF) receptor I (sTNFR-I) constructs were evaluated in juvenile baboons. The constructs included either an sTNFR-I IgG1 immunoadhesin (p55 sTNFR-I Fc) or five different sTNFR-I constructs covalently linked to polyethylene glycol. The constructs were administered intravenously three times, and pharmacokinetics and immunogenicity were examined over 63 days. All of the constructs were immunogenic, with the exception of a 2.6-domain monomeric sTNFR-I. To evaluate whether the nonimmunogenic 2.6-domain monomeric construct could protect baboons against TNF-α-induced mortality, baboons were pretreated with 1, 5, or 10 mg/kg body wt and were compared with baboons receiving either placebo or 1 mg/kg body wt of the dimeric 4.0-domain sTNFR-I construct ( n = 3 each) before lethal Escherichia colibacteremia. The monomeric construct protected baboons and neutralized TNF bioactivity, although greater quantities were required compared with the dimeric 4.0-domain sTNFR-I construct. We conclude that E. coli-recombinant-derived human sTNFR-I constructs can be generated with minimal immunogenicity on repeated administration and still protect against the consequences of exaggerated TNF-α production.

Central endothelin ETBreceptors mediate IL-1-dependent fever induced by preformed pyrogenic factor and corticotropin-releasing factor in the rat

2006 ◽  
Vol 290 (1) ◽  
pp. R164-R171 ◽  
Author(s):  
Aline S. C. Fabricio ◽  
Giles A. Rae ◽  
Aleksander R. Zampronio ◽  
Pedro D'Orléans-Juste ◽  
Glória E. P. Souza
Keyword(s):  
Receptor Antagonist ◽  
Corticotropin Releasing Factor ◽  
Tnf Receptor ◽  
Conscious Rats ◽  
Tnf Α ◽  
Soluble Tnf Receptor ◽  
The Brain ◽  
Tnf Receptor I

Blockade of central endothelin ETBreceptors inhibits fever induced by LPS in conscious rats. The contribution of ETBreceptor-mediated mechanisms to fever triggered by intracerebroventricular IL-6, PGE2, PGF2α, corticotropin-releasing factor (CRF), and preformed pyrogenic factor derived from LPS-stimulated macrophages (PFPF) was examined. The influence of natural IL-1 receptor antagonist or soluble TNF receptor I on endothelin (ET)-1-induced fever was also assessed. The selective ETBreceptor antagonist BQ-788 (3 pmol icv) abolished fever induced by intracerebroventricular ET-1 (1 pmol) or PFPF (200 ng) and reduced that caused by ICV CRF (1 nmol) but not by IL-6 (14.6 pmol), PGE2(1.4 nmol), or PGF2α(2 nmol). CRF-induced fever was also attenuated by bosentan (dual ETA/ETBreceptor antagonist; 10 mg/kg iv) but unaffected by BQ-123 (selective ETAreceptor antagonist; 3 pmol icv). α-Helical CRF9–41(dual CRF1/CRF2receptor antagonist; 6.5 nmol icv) attenuated fever induced by CRF but not by ET-1. Human IL-1 receptor antagonist (9.1 pmol) markedly reduced fever to IL-1β (180 fmol) or ET-1 and attenuated that caused by PFPF or CRF. Murine soluble TNF receptor I (23.8 pmol) reduced fever to TNF-α (14.7 pmol) but not to ET-1. The results of the present study suggest that PFPF and CRF recruit the brain ET system to cause ETBreceptor-mediated IL-1-dependent fever.

scholarly journals The roles of TNF-α and the soluble TNF receptor I on sleep architecture in OSA

2009 ◽  
Vol 13 (3) ◽  
pp. 263-269 ◽  
Author(s):  
Herbert J. Yue ◽  
Paul J. Mills ◽  
Sonia Ancoli-Israel ◽  
José S. Loredo ◽  
Michael G. Ziegler ◽  
...  
Keyword(s):  
Sleep Architecture ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Soluble Tnf Receptor ◽  
Tnf Receptor I

Pharmacokinetics, immunogenicity, and efficacy of dimeric TNFR binding proteins in healthy and bacteremic baboon

1998 ◽  
Vol 84 (4) ◽  
pp. 1119-1130 ◽  
Author(s):  
Carmen C. Solorzano ◽  
Atsushi Kaibara ◽  
Phillip J. Hess ◽  
Paul D. Edwards ◽  
Riadh Ksontini ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Polyethylene Glycol ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tnf Receptor ◽  
E Coli ◽  
Cytokine Responses ◽  
Tnf Α ◽  
Tnf Receptor I ◽  
Necrosis Factor

Immunogenicity, pharmacokinetics, and therapeutic efficacy of three novel dimeric soluble tumor necrosis factor (TNF)-receptor I constructs [TNF-binding protein (bp)] were evaluated in 28 baboons, 12 of which were healthy and 16 were challenged with a lethal Escherichia coli bacteremia. The three constructs differed only in the number of extracellular domains of the TNF receptor I and were dimerized with polyethylene glycol. Although all three constructs had generally similar pharmacokinetics when administered to a naive animal, they differed quantitatively in their immunogenicity. Antibodies were detected more frequently, and titers were significantly higher ( P < 0.05) in both healthy and septic baboons that received the 4.0-domain TNF-bp construct, compared with animals receiving the 2.6-domain construct. When the TNF-bp constructs were administered a second time (21 days later), the half-lives of the three constructs were significantly shorter in animals that had an antibody response after the first injection. In contrast, all three TNF-bp constructs were equally effective at improving outcome, blocking a systemic TNF-α response, and attenuating the cytokine responses when administered at a dose of 1.0 mg/kg body wt 1 h before a lethal E. coli infusion. The findings suggest that immunogenicity of TNF-bp constructs can be altered by changing the number of functional domains, without affecting their capacity to neutralize TNF-α and to abrogate TNF-mediated pathology.

Tumor necrosis factor receptor-mediated apoptosis in Trichinella spiralis-infected muscle cells

Parasitology ◽  
2005 ◽  
Vol 131 (3) ◽  
pp. 373-381 ◽  
Author(s):  
Z. WU ◽  
I. NAGANO ◽  
T. BOONMARS ◽  
Y. TAKAHASHI
Keyword(s):  
Caspase 3 ◽  
Trichinella Spiralis ◽  
Cell Formation ◽  
Muscle Cells ◽  
Cyst Formation ◽  
Signalling Pathway ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Infected Muscle ◽  
Necrosis Factor

In order to reveal the mechanisms underlying nurse cell formation during Trichinella spiralis infection, the expression of the factors of tumor necrosis factor-alpha (TNF-α)/TNF receptor 1 (TNFR-1) signalling pathway mediating apoptosis was investigated. The analysed factors included TNF-α, TNFR-1, TNF receptor-associated death-domain (TRADD), caspase 3, caspase 8, TNF receptor associated factor-2 (TRAF2) and receptor interactive protein (RIP), all of which are involved in the TNF-α/TNFR-1 signalling pathway-mediated apoptosis. The quantitative RT-PCR indicated that the infected muscle tissues up-regulate the expression of pro-apoptosis genes (TNF-α, TNFR-1 and TRADD, caspase 3 and caspase 8), and anti-apoptosis genes (TRAF2 and RIP) at the beginning of cyst formation. The expression returned to the normal level after cyst formation. The quantitative RT-PCR analysis of mRNA from tissue samples isolated by laser capture micro-dissection confirmed that the up-regulation of these genes was restricted in infected muscle cells, was not in the inflammation cells around infected muscle cells nor in normal muscle cells. The in situ localization study of pro-apoptosis (TRADD, caspase 3) and anti-apoptosis gene products (TRAF2) indicated that these were expressed in the basophilic cytoplasm (infected muscle cell origin) of the nurse cells. Thus the present study suggests that the TNF-α/TNFR-1 signalling pathway is involved in nurse cell formation.

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