Journal
JOURNAL OF IMMUNOLOGY
Volume 174, Issue 11, Pages 6791-6802Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.11.6791
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Funding
- NIAID NIH HHS [AI46653, AI42767, T32AI0726-19, AI50073] Funding Source: Medline
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IFN-gamma plays a critical role in the CD8(+) T cell response to infection, but when and if this cytokine directly signals CD8+ T cells during an immune response is unknown. We show that naive Ag-specitic CD8(+) T cells receive IFN-gamma signals within 12 h after in vivo infection with Listeria monocytogenes and then become unresponsive to IFN-gamma throughout the ensuing Ag-driven expansion phase. Ag-specific CD8(+) T cells regain partial IFN-gamma responsiveness throughout the contraction phase, whereas the memory pool exhibits uniform, but reduced, responsiveness that is also modulated during the secondary response. The responsiveness of Ag-specific CD8(+) T cells to IFN-gamma correlated with modulation in the expression of IFN-gamma R2, but not with IFN-gamma R1 or suppressor of cytokine signaling-1. This dynamic regulation suggests that early IFN-gamma signals participate in regulation of the primary CD8(+) T cell response program, but that evading or minimizing IFN-y signals during expansion and the memory phase may contribute to appropriate regulation of the CD8(+) T cell response.
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