作者: Warren S Alexander , Robyn Starr , Jennifer E Fenner , Clare L Scott , Emanuela Handman
DOI: 10.1016/S0092-8674(00)80047-1
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摘要: Mice lacking suppressor of cytokine signaling-1 (SOCS1) develop a complex fatal neonatal disease. In this study, SOCS1-/- mice were shown to exhibit excessive responses typical those induced by interferon gamma (IFNgamma), hyperresponsive viral infection, and yielded macrophages with an enhanced IFNgamma-dependent capacity kill L. major parasites. The disease in was prevented administration anti-IFNgamma antibodies did not occur also the IFNgamma gene. Although is essential for resistance variety infections, potential toxic action IFNgamma, particularly mice, appears require regulation. Our data indicate that SOCS1 key modulator action, allowing protective effects without risk associated pathological responses.