Biomaterial Database

Suppression of antiviral responses by antibody-dependent enhancement of macrophage infection. 2003

Andreas Suhrbier, and May La Linn

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

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.

UI	MeSH Term	Description	Entries
D008264	Macrophages	The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)	Bone Marrow-Derived Macrophages,Monocyte-Derived Macrophages,Macrophage,Macrophages, Monocyte-Derived,Bone Marrow Derived Macrophages,Bone Marrow-Derived Macrophage,Macrophage, Bone Marrow-Derived,Macrophage, Monocyte-Derived,Macrophages, Bone Marrow-Derived,Macrophages, Monocyte Derived,Monocyte Derived Macrophages,Monocyte-Derived Macrophage
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D012327	RNA Virus Infections	Diseases caused by RNA VIRUSES.	Infections, RNA Virus,Infection, RNA Virus,RNA Virus Infection,Virus Infection, RNA,Virus Infections, RNA
D012328	RNA Viruses	Viruses whose genetic material is RNA.	RNA Rodent Viruses,RNA Rodent Virus,RNA Virus,Rodent Virus, RNA,Rodent Viruses, RNA,Virus, RNA,Virus, RNA Rodent,Viruses, RNA,Viruses, RNA Rodent
D015398	Signal Transduction	The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.	Cell Signaling,Receptor-Mediated Signal Transduction,Signal Pathways,Receptor Mediated Signal Transduction,Signal Transduction Pathways,Signal Transduction Systems,Pathway, Signal,Pathway, Signal Transduction,Pathways, Signal,Pathways, Signal Transduction,Receptor-Mediated Signal Transductions,Signal Pathway,Signal Transduction Pathway,Signal Transduction System,Signal Transduction, Receptor-Mediated,Signal Transductions,Signal Transductions, Receptor-Mediated,System, Signal Transduction,Systems, Signal Transduction,Transduction, Signal,Transductions, Signal
D016753	Interleukin-10	A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.	IL-10,CSIF-10,Cytokine Synthesis Inhibitory Factor,IL10,Interleukin 10
D017452	Receptors, IgG	Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).	Antigens, CD16,Antigens, CD32,Antigens, CD64,CD16 Antigens,CD32 Antigens,CD64 Antigen,CD64 Antigens,Fc Gamma Receptor,Fc Receptors, gamma,Fc gamma Receptors,IgG Receptor,IgG Receptors,Leu-11 Antigen,Receptors, Fc gamma,gamma Fc Receptor,gamma Fc Receptors,CD 16 Antigens,CD 32 Antigens,CD 64 Antigens,CDw32 Antigens,Fc gamma RI,Fc gamma RII,Fc gamma RIII,Immunoglobulin G Receptor,Leu-11 Antigens,Antigen, CD64,Antigen, Leu-11,Antigens, CD 16,Antigens, CD 32,Antigens, CD 64,Antigens, CDw32,Antigens, Leu-11,Fc Receptor, gamma,Gamma Receptor, Fc,Leu 11 Antigen,Leu 11 Antigens,Receptor, Fc Gamma,Receptor, IgG,Receptor, Immunoglobulin G,Receptor, gamma Fc,Receptors, gamma Fc,gamma RI, Fc,gamma RII, Fc,gamma RIII, Fc,gamma Receptors, Fc
D019067	Antibody-Dependent Enhancement	Enhancement of viral infectivity caused by non-neutralizing antibodies. There are at least two mechanisms known to account for this: mediation by Fc receptors (RECEPTORS, FC) or by complement receptors (RECEPTORS, COMPLEMENT). Either the virus is complexed with antiviral IMMUNOGLOBULIN G and binds to Fc receptors, or virus is coated with antiviral IMMUNOGLOBULIN M and binds to complement receptors.	Antibody Dependent Enhancement,Antibody-Dependent Enhancements,Enhancement, Antibody-Dependent