How both apoptotic death and immunity may be triggered by dsRNA
How both apoptotic death and immunity may be triggered by dsRNA. The cellular ‘death-inducing’ events after exposure to dsRNA – following virus infection or vaccination – include the RNaseL and PKR pathways, which destroy mRNA and stop translation, respectively. Though the mechanisms are not fully known, apoptosis is induced in part by enhancing efficiency in the transmission of death signals through the adaptor, FADD, and enhanced activity of the death-induced signaling complex (DISC) [,]. Two proapoptotic members of the Bcl-2 family, Bad and Bax, are also induced. The PKR pathway can be activated (phosphorylated; this is indicated by the asterisks) by an endogenous gene product called Pact or inhibited by a variety of viral and cellular inhibitors that can act at a number of points in the pathway; these are summarized in []. Activated PKR also induces NF-κB and a variety of molecules that facilitate T cell recognition of infected targets (red box). LPS, lipopolysaccharide; syn., sythetase; TAP, transporter associated with antigen processing.