Effector Molecules and CTL Homeostasis
Chapters 7, 8, and 9 have discussed effector molecules in relation to their direct antiviral activity: to kill infected cells or to inhibit the spread of the virus from cell to cell by nonlytic means. We discussed the role of the different types of effector mechanisms for the successful resolution of infection, and how the exact balance between lytic and nonlytic effector mechanisms can determine whether pathology is observed or not. However, experimental data indicate that the effector molecules might have a broader function than just antiviral activity [(2000)]. In addition, they might serve as regulatory molecules that determine the extent to which the population of CTL expands in response to antigenic stimulation. Experimental data indicate that the amount of effector molecules that are secreted by CTL can influence the peak size of the CTL response, as well as the number of CTL found in the memory phase after the infection has been resolved. Of particular interest in this respect are mice that have deficiencies in either perforin or IFN-γ. Perforin is the main effector molecule that is responsible for CTL-mediated lysis, while IFN-γ is known to be a CTL-secreted soluble mediator that inhibits viral replication in several infections, for example LCMV. A deficiency in either perforin or IFN-γ, or both, has been observed to result in higher levels of CTL both in the acute and the post acute phase of infections [(2000); (1999); (2000)].
KeywordsVirus Load Vesicular Stomatitis Virus Antigenic Stimulation Direct Antiviral Activity Reduce Virus Load
Unable to display preview. Download preview PDF.