| First Author | Barnes N | Year | 2002 |
| Journal | Immunity | Volume | 16 |
| Issue | 3 | Pages | 379-89 |
| PubMed ID | 11911823 | Mgi Jnum | J:86281 |
| Mgi Id | MGI:2679189 | Doi | 10.1016/s1074-7613(02)00287-x |
| Citation | Barnes N, et al. (2002) FcgammaRI-deficient mice show multiple alterations to inflammatory and immune responses. Immunity 16(3):379-89 |
| abstractText | 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. |
