Abstract
The host response to viral infection consists of both virus-specific and nonspecific elements. Among the specific (immune mediated) responses to viral infection, several lines of evidence point toward the cytolytic T lymphocyte (CTL) as an important effector in antiviral immunity [1]. Notably, specific antiviral cell-mediated cytolytic activity is readily demonstrable during the course of many experimental viral infections [2]. More importantly, both heterogeneous and cloned populations of antiviral CTL have been shown, upon adoptive in vivo transfer into infected recipients, to specifically inhibit virus replication and to alter the outcome of lethal infection [2–5]. Because the antiviral activity of this T lymphocyte subset is monitored in vitro by the capacity of sensitized CTL to directly destroy virally infected target cells by cell-to-cell contact [1], it is reasonable to assume that CTL would function in a similar manner in vivo to eliminate virus, i.e., by direct destruction of infected cells. However, antiviral CTL have also been shown to release lymphokines, including interferon-γ (IFNγ), after contact with antigen [6]. Thus, CTL may inhibit, through a variety of mechanisms (both antigen-specific and nonspecific), virus replication and spread in the body [7].
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Braciale, T.J., Braciale, V.L. (1986). CTL Recognition of Transfected H-2 Gene and Viral Gene Products. In: Notkins, A.L., Oldstone, M.B.A. (eds) Concepts in Viral Pathogenesis II. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-4958-0_20
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DOI: https://doi.org/10.1007/978-1-4612-4958-0_20
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