期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 2, 页码 999-1006出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.2.999
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资金
- NCI NIH HHS [R01 CA 109446] Funding Source: Medline
- NIAID NIH HHS [R01 AI 42767, P01 AI 60699, R01 AI 46653, R01 AI 50073, R01 AI 059752] Funding Source: Medline
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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