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TRAIL Deficiency Delays, but Does Not Prevent, Erosion in the Quality of "Helpless" Memory CD8 T Cells¹

Vladimir P. Badovinac^*, Kelly A. Nordyke Messingham^*, Thomas S. Griffith and John T. Harty^2,*,

^* Department of Microbiology, Department of Urology, and Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242

In this study, we investigated the role of TRAIL in Ag-specific CD8 T cell homeostasis after viral infection. TRAIL deficiency does not influence the kinetics of the Ag-specific CD8 T cell responses, and CD8 T cells in TRAIL-deficient mice were able to expand, contract, and generate functional memory cell numbers that were indistinguishable from TRAIL-sufficient wild-type CD8 T cells after acute lymphocytic choriomeningitis virus infection. Interestingly, the ability of "helpless" CD8 T cells to retain their memory phenotypic and functional (i.e., secondary expansion) characteristics was prolonged in TRAIL-deficient mice compared with wild-type CD4-depleted controls. However, TRAIL deficiency only delayed, but did not prevent, the eventual erosion in the quality of helpless memory CD8 T cells, and that correlated with their inability to respond to a second round of Ag-driven proliferation. These data, which suggest that CD4 help consists of both TRAIL-dependent and -independent components, may help to resolve the current controversy between the early programming and maintenance models that were put forward to explain the role of CD4 T cell help in Ag-specific CD8 T cell homeostasis.

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The JI 2006 177: 767-768. [Full Text]  

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