Suppression of antiviral responses by antibody-dependent enhancement of macrophage infection.
Antibody-dependent enhancement (ADE) of macrophage and monocyte infection has been demonstrated in vitro for some of the most deadly RNA viruses known. Recent evidence suggests that ADE-mediated ligation of Fc receptors might suppress host-cell antiviral gene expression by promoting early interleukin-10 (IL-10) secretion, resulting in the expression of suppressor-of-cytokine-signalling (SOCS) proteins and a Th2 bias. These findings provide potential new insights into how ADE might enhance viral infections and exacerbate disease.
Suhrbier
Andreas
A
Queensland Institute of Medical Research and the Australian Centre for International & Tropical Health & Nutrition, 300 Herston Road, Herston, Queensland 4029, Australia. andreasS@qimr.edu.au
La Linn
May
M
D019067:Antibody-Dependent Enhancement / Q000276:immunology*; D006801:Humans; D016753:Interleukin-10 / Q000276:immunology / Q000378:metabolism; D008264:Macrophages / Q000276:immunology* / Q000821:virology*; D012327:RNA Virus Infections / Q000276:immunology; D012328:RNA Viruses / Q000276:immunology*; D017452:Receptors, IgG / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction
C445323:FCGR2A protein, human; C499173:FCGR2B protein, human; D017452:Receptors, IgG; D016753:Interleukin-10