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Nat Rev Immunol. 2011 Dec 23;12(2):79-88. doi: 10.1038/nri3131.

Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways.

Author information

Department of Microbiology and Immunology, Emory Vaccine Center, 1462 Clifton Rd. NE, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Section of Molecular Genetics and Microbiology, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin 78712, USA.
Contributed equally


Pathogens specifically target both the caspase 8-dependent apoptotic cell death pathway and the necrotic cell death pathway that is dependent on receptor-interacting protein 1 (RIP1; also known as RIPK1) and RIP3 (also known as RIPK3). The fundamental co-regulation of these two cell death pathways emerged when the midgestational death of mice deficient in FAS-associated death domain protein (FADD) or caspase 8 was reversed by elimination of RIP1 or RIP3, indicating a far more entwined relationship than previously appreciated. Thus, mammals require caspase 8 activity during embryogenesis to suppress the kinases RIP1 and RIP3 as part of the dialogue between two distinct cell death processes that together fulfil reinforcing roles in the host defence against intracellular pathogens such as herpesviruses.

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