Priming of neutrophils with tumor necrosis factor-α measured as Fcγ receptor-mediated respiratory burst correlates with increased complement receptor 3 membrane density

1996 ◽  
Vol 26 (4) ◽  
pp. 236-239 ◽  
Author(s):  
B. Åsman ◽  
A. Gustafsson ◽  
K. Bergström
Keyword(s):  
Tumor Necrosis Factor ◽  
Respiratory Burst ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Complement Receptor ◽  
Fcγ Receptor ◽  
Complement Receptor 3 ◽  
Factor Α ◽  
Membrane Density ◽  
Necrosis Factor

scholarly journals Fcγ receptor type IIIA genotype and response to tumor necrosis factor α–blocking agents in patients with rheumatoid arthritis

2007 ◽  
Vol 56 (2) ◽  
pp. 448-452 ◽  
Author(s):  
Alf Kastbom ◽  
Johan Bratt ◽  
Sofia Ernestam ◽  
Jon Lampa ◽  
Leonid Padyukov ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Receptor Type ◽  
Fcγ Receptor ◽  
Blocking Agents ◽  
Type Iiia ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Fcγ-receptor signaling augments the LPS-stimulated increase in serum tumor necrosis factor-α levels

2001 ◽  
Vol 280 (4) ◽  
pp. R1037-R1044 ◽  
Author(s):  
Marion L. Refici ◽  
Dennis W. Metzger ◽  
Bernard P. Arulanandam ◽  
Michelle R. Lennartz ◽  
Daniel J. Loegering
Keyword(s):  
Tumor Necrosis Factor ◽  
Complement Activation ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Fcγ Receptor ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

The phagocytosis of IgG-coated erythrocytes (EIgG) has been shown to augment the bacterial lipopolysaccharide (LPS)-stimulated increase in serum tumor necrosis factor-α (TNF-α) levels. The present study evaluated the role of Fcγ-receptor (FcγR) signaling and complement activation in the effect of EIgG on the TNF-α response to LPS. The role of FcγR was determined using FcR γ-chain knockout mice that lack functional FcγRI and FcγRIII. In wild-type animals, EIgG caused a 16-fold augmentation of the serum TNF-α response to LPS, whereas there was no augmentation in the FcγR-deficient animals. Heat-damaged erythrocytes also augmented the TNF-α response to LPS. This effect was absent in FcγR-deficient animals. An IgG antibody against heated erythrocytes was detected in mouse serum. The complement activation caused by EIgG had little effect on the LPS-stimulated increase in serum TNF-α levels as indicated by activation of complement with cobra venom factor or IgM-coated erythrocytes as well as studies with C5-deficient mice. These results indicate that FcγR signaling primarily mediates the augmented serum TNF-α response to LPS caused by EIgG.

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