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

Marion L. Refici, Dennis W. Metzger, Bernard P. Arulanandam, Michelle R. Lennartz, Daniel J. Loegering

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)R1037-R1044
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number4 49-4
StatePublished - 2001
Externally publishedYes


  • C5 knockout mice
  • Cobra venom factor
  • Complement activation
  • Fc receptor γ-chain knockout mice
  • Heat-damaged erythrocytes
  • Sepsis

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


Dive into the research topics of 'Fcγ-receptor signaling augments the LPS-stimulated increase in serum tumor necrosis factor-α levels'. Together they form a unique fingerprint.

Cite this