FcγRI-deficient mice show multiple alterations to inflammatory and immune responses

Nadine Barnes, Amanda L. Gavin, Peck Szee Tan, Patricia Mottram, Frank Koentgen, P. Mark Hogarth

Research output: Contribution to journalArticleResearchpeer-review

165 Citations (Scopus)


The inactivation of the mouse high-affinity IgG Fc receptor FcγRI resulted in a wide range of defects in antibody Fc-dependent functions. These studies showed the primary importance of FcγRI 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 FcγRI, antibody responses were elevated, implying the removal of a control point by the deletion of FcγRI. In addition, FcR-γ chain-deficient mice were found to express partially functional FcγRI. Thus, FcγRI is an early participant in Fc-dependent cell activation and in the development of immune responses.

Original languageEnglish
Pages (from-to)379-389
Number of pages11
Issue number3
Publication statusPublished - 1 Jan 2002
Externally publishedYes

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