TRAIL deficiency delays, but does not prevent, erosion in the quality of "helpless" memory CD8 T cells

Vladimir P. Badovinac, Kelly A. Nordyke Messingham, Thomas S. Griffith, John T. Harty

Research output: Contribution to journalArticlepeer-review

50 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)999-1006
Number of pages8
JournalJournal of Immunology
Volume177
Issue number2
DOIs
StatePublished - Jul 15 2006

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