| First Author | Fransen MF | Year | 2018 |
| Journal | J Immunol | Volume | 200 |
| Issue | 8 | Pages | 2615-2626 |
| PubMed ID | 29523656 | Mgi Jnum | J:264675 |
| Mgi Id | MGI:6152153 | Doi | 10.4049/jimmunol.1700429 |
| Citation | Fransen MF, et al. (2018) A Restricted Role for FcgammaR in the Regulation of Adaptive Immunity. J Immunol 200(8):2615-2626 |
| abstractText | By their interaction with IgG immune complexes, FcgammaR and complement link innate and adaptive immunity, showing functional redundancy. In complement-deficient mice, IgG downstream effector functions are often impaired, as well as adaptive immunity. Based on a variety of model systems using FcgammaR-knockout mice, it has been concluded that FcgammaRs are also key regulators of innate and adaptive immunity; however, several of the model systems underpinning these conclusions suffer from flawed experimental design. To address this issue, we generated a novel mouse model deficient for all FcgammaRs (FcgammaRI/II/III/IV(-/-) mice). These mice displayed normal development and lymphoid and myeloid ontogeny. Although IgG effector pathways were impaired, adaptive immune responses to a variety of challenges, including bacterial infection and IgG immune complexes, were not. Like FcgammaRIIb-deficient mice, FcgammaRI/II/III/IV(-/-) mice developed higher Ab titers but no autoantibodies. These observations indicate a redundant role for activating FcgammaRs in the modulation of the adaptive immune response in vivo. We conclude that FcgammaRs are downstream IgG effector molecules with a restricted role in the ontogeny and maintenance of the immune system, as well as the regulation of adaptive immunity. |
