title: FcgammaRI-deficient mice show multiple alterations to inflammatory and immune responses.
abstract: The inactivation of the mouse high-affinity IgG Fc receptor FcgammaRI resulted in a wide range of defects in antibody Fc-dependent functions. These studies showed the primary importance of FcgammaRI in endocytosis of monomeric IgG, kinetics, and extent of phagocytosis of immune complexes, in macrophage-based ADCC, and in immune complex-dependent antigen presentation to primed T cells. In the absence of FcgammaRI, antibody responses were elevated, implying the removal of a control point by the deletion of FcgammaRI. In addition, FcR-gamma chain-deficient mice were found to express partially functional FcgammaRI. Thus, FcgammaRI is an early participant in Fc-dependent cell activation and in the development of immune responses.
authors.affiliation: The Austin Research Institute, Kronheimer Building, Studley Road, Heidelberg, Victoria 3084, Australia.
authors.forename: Nadine
authors.initials: N
authors.lastname: Barnes
authors.forename: Amanda L
authors.initials: AL
authors.lastname: Gavin
authors.forename: Peck Szee
authors.initials: PS
authors.lastname: Tan
authors.forename: Patricia
authors.initials: P
authors.lastname: Mottram
authors.forename: Frank
authors.initials: F
authors.lastname: Koentgen
authors.forename: P Mark
authors.initials: PM
authors.lastname: Hogarth
mesh_terms: D000818:Animals; D017353:Gene Deletion; D007109:Immunity / Q000235:genetics; D007249:Inflammation / Q000235:genetics; D008213:Lymphocyte Activation / Q000235:genetics / Q000276:immunology; D051379:Mice; D017452:Receptors, IgG / Q000172:deficiency / Q000235:genetics* / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D017452:Receptors, IgG