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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. FcgammaRI-deficient mice show multiple alterations to inflammatory and immune responses. Barnes, N., Gavin, A.L., Tan, P.S., Mottram, P., Koentgen, F., Hogarth, P.M. Immunity (2002) [Pubmed]
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