| First Author | Rojo S | Year | 2000 |
| Journal | Mol Cell Biol | Volume | 20 |
| Issue | 19 | Pages | 7178-82 |
| PubMed ID | 10982834 | Mgi Jnum | J:64504 |
| Mgi Id | MGI:1889426 | Doi | 10.1128/mcb.20.19.7178-7182.2000 |
| Citation | Rojo S, et al. (2000) Natural killer cells and mast cells from gp49B null mutant mice are functional. Mol Cell Biol 20(19):7178-82 |
| abstractText | Immune responses are controlled by a combination of positive and negative cellular signals. Effector cells in the immune system express inhibitory receptors that serve to limit effector cell expansion and to protect the host from autoreactivity. gp49B is a receptor of unknown function that is expressed on activated mast cells and natural killer (NK) cells and whose cytoplasmic tail endows it with inhibitory potential. To gain insight into the function of gp49B in mice, we disrupted the gp49B gene by homologous recombination. gp49B(0) mice were born at expected ratios, were healthy and fertile, and displayed normal long-term survival rates. gp49B(0) mice showed no defect in NK or mast cell development. Furthermore, NK and mast cells from the gp49B(0) mice showed activation properties in vitro similar to those of cells isolated from wild-type mice. Therefore, gp49B is not critical for the development, expansion, and maturation of mast cells and NK cells in vivo. The healthy status of gp49B(0) mice makes them suitable for testing the role of gp49B in immune responses to infectious agents. |
