Staying alive: cell death in antiviral immunity.
Programmed cell death is an integral part of host defense against invading intracellular pathogens. Apoptosis, programmed necrosis, and pyroptosis each serve to limit pathogen replication in infected cells, while simultaneously promoting the inflammatory and innate responses that shape effective long-term host immunity. The importance of carefully regulated cell death is evident in the spectrum of inflammatory and autoimmune disorders caused by defects in these pathways. Moreover, many viruses encode inhibitors of programmed cell death to subvert these host responses during infection, thereby facilitating their own replication and persistence. Thus, as both virus and cell vie for control of these pathways, the battle for survival has shaped a complex host-pathogen interaction. This review will discuss the multifaceted role that programmed cell death plays in maintaining the immune system and its critical function in host defense, with a special emphasis on viral infections.
Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA. Electronic address: upton@austin.utexas.edu.
Jason W
JW
Upton
Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: francis.chan@umassmed.edu.
Francis Ka-Ming
FK
Chan
D000818:Animals; D016923:Cell Death / Q000276:immunology; D054884:Host-Pathogen Interactions / Q000276:immunology*; D008214:Lymphocytes / Q000276:immunology / Q000821:virology; D008322:Mammals / Q000821:virology*; D018448:Models, Immunological; D014777:Virus Diseases / Q000276:immunology*