| First Author | Ishii S | Year | 1998 |
| Journal | J Exp Med | Volume | 187 |
| Issue | 11 | Pages | 1779-88 |
| PubMed ID | 9607919 | Mgi Jnum | J:88505 |
| Mgi Id | MGI:3033561 | Doi | 10.1084/jem.187.11.1779 |
| Citation | Ishii S, et al. (1998) Impaired anaphylactic responses with intact sensitivity to endotoxin in mice lacking a platelet-activating factor receptor. J Exp Med 187(11):1779-88 |
| abstractText | Platelet-activating factor (PAF) is a potent phospholipid mediator with diverse biological activities in addition to its well-known ability to stimulate platelet aggregation. Pharmacologic studies had suggested a role for PAF in pregnancy, neuronal cell migration, anaphylaxis, and endotoxic shock. Here we show that disruption of the PAF receptor gene in mice caused a marked reduction in systemic anaphylactic symptoms. Unexpectedly, however, the PAF receptor-deficient mice developed normally, were fertile, and remained sensitive to bacterial endotoxin. These mutant mice clearly show that PAF plays a dominant role in eliciting anaphylaxis, but that it is not essential for reproduction, brain development, or endotoxic shock. |
