摘要
Salmonella enteric strains are facultat- ive intracellular pathogens that canproduce both localized enteritis and dis- seminated systemic disease in humans and a variety of other vertebrates.1 Extensive evidence obtained from genetic and cell biology studies indicates that Salmonella has evolved specific virulence mechanisms to evade innate immune responses.1 However, the underlying molecular and cellular mechanisms have not been under- stood very well. A recent paper published by Robinson et al. in Nature Immunology2 reported that type I interferon （IFN）- induced macrophage necroptosis plays a critical role in evading host innate immune responses during infection with
Salmonella enteric strains are facultat- ive intracellular pathogens that canproduce both localized enteritis and dis- seminated systemic disease in humans and a variety of other vertebrates.1 Extensive evidence obtained from genetic and cell biology studies indicates that Salmonella has evolved specific virulence mechanisms to evade innate immune responses.1 However, the underlying molecular and cellular mechanisms have not been under- stood very well. A recent paper published by Robinson et al. in Nature Immunology2 reported that type I interferon （IFN）- induced macrophage necroptosis plays a critical role in evading host innate immune responses during infection with
