After resolved viral liver infection, virus-specific liver CD8
+ T cells separated into liver-resident CXCR6
hi and circulating CX
3CR1
+ memory T cells. CXCR6
hi T cells were present also during persistent viral liver infection, in contrast to absent CX
3CR1
+ T
EM cells. However, these CXCR6
hi T cells were dysfunctional, and their gene expression dominated by the transcription factor CREM/ICER. Enhanced cAMP signaling upstream of CREM/ICER hampered functionality, which was partially restored in ICER-deficient T cells. Hence, targeting cAMP signaling may be a promising strategy to reinvigorate dysfunctional resident T cells.
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After resolved viral liver infection, virus-specific liver CD8
+ T cells separated into liver-resident CXCR6
hi and circulating CX
3CR1
+ memory T cells. CXCR6
hi T cells were present also during persistent viral liver infection, in contrast to absent CX
3CR1
+ T
EM cells. However, these CXCR6
hi T cells were dysfunctional, and their gene expression dominated by the transcription factor CREM/ICER. Enhanced cAMP signaling upstream of CREM/ICER hampered functionality, which was partially restored in ICER-d...
»