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-/- Mice Develop Functionally Impaired CD8+ T Cell Responses and Fail to Contain Virus Infection of the Central Nervous System
*
Department of Microbiology, University of Tennessee, Knoxville, TN 37996; and
Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033
Recent observations have indicated that viral persistence and tumor
spreading could occur because of effector function-defective
CD8+ T cells. Although chronic exposure to Ag, lack of CD4
help, and epitope dominance are suggested to interfere with CTL
differentiation, mechanisms underlying the defective effector function
remain obscure. We demonstrate in this report that lymphotoxin
-deficient mice develop CD8+ T cells at normal
frequencies when infected with HSV or immunized with OVA Ag but show
impaired cytotoxic and cytokine-mediated effector functions resulting
in enhanced susceptibility to HSV-induced encephalitis. Although these
cells display near normal levels of perforin and Fas ligand, they
remain largely at a naive state as judged by high expression of CD62
ligand and failure to up-regulate activation or memory markers. In
particular, these CD8+ T cells revealed inadequate
expression of the IL-12 receptor, thus establishing a link between CTL
differentiation and LT possibly through regulation of IL-12
receptor. Viruses and tumors could evade immunity by targeting the same
pathway.
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