| First Author | Refici ML | Year | 2001 |
| Journal | Am J Physiol Regul Integr Comp Physiol | Volume | 280 |
| Issue | 4 | Pages | R1037-44 |
| PubMed ID | 11247825 | Mgi Jnum | J:114295 |
| Mgi Id | MGI:3688707 | Doi | 10.1152/ajpregu.2001.280.4.R1037 |
| Citation | Refici ML, et al. (2001) Fcgamma-receptor signaling augments the LPS-stimulated increase in serum tumor necrosis factor-alpha levels. Am J Physiol Regul Integr Comp Physiol 280(4):R1037-44 |
| abstractText | The phagocytosis of IgG-coated erythrocytes (EIgG) has been shown to augment the bacterial lipopolysaccharide (LPS)-stimulated increase in serum tumor necrosis factor-alpha (TNF-alpha) levels. The present study evaluated the role of Fcgamma-receptor (FcgammaR) signaling and complement activation in the effect of EIgG on the TNF-alpha response to LPS. The role of FcgammaR was determined using FcR gamma-chain knockout mice that lack functional FcgammaRI and FcgammaRIII. In wild-type animals, EIgG caused a 16-fold augmentation of the serum TNF-alpha response to LPS, whereas there was no augmentation in the FcgammaR-deficient animals. Heat-damaged erythrocytes also augmented the TNF-alpha response to LPS. This effect was absent in FcgammaR-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-alpha 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 FcgammaR signaling primarily mediates the augmented serum TNF-alpha response to LPS caused by EIgG. |
