Publication in detail

Immunity 2002 Mar;16(3):379

FcgammaRI-deficient mice show multiple alterations to inflammatory and immune responses.

Barnes, N; Gavin, AL; Hogarth, PM.; Koentgen, F; Mottram, P; Tan, PS

Kronheimer Building, Studley Road, Heidelberg, Victoria 3084, Australia.

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.

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