Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 203, Issue 10, Pages 2263-2269Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20060995
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Funding
- NCI NIH HHS [R01 CA071971, R01CA100644, F32 CA106090, F32CA106090, R01CA71971, R01 CA100644] Funding Source: Medline
- NIAID NIH HHS [R01 AI040519, R37 AI030048, P01AI44644, R37AI30048, R01AI040519, P01 AI044644] Funding Source: Medline
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Numerous microbes establish persistent infections, accompanied by antigen-specific CD8 T cell activation. Pathogen-specific T cells in chronically infected hosts are often phenotypically and functionally variable, as well as distinct from T cells responding to nonpersistent infections; this phenotypic heterogeneity has been attributed to an ongoing reencounter with antigen. Paradoxically, maintenance of memory CD8 T cells to acutely resolved infections is antigen independent, whereas there is a dependence on antigen for T cell survival in chronically infected hosts. Using two chronic viral infections, we demonstrate that new naive antigen-specific CD8 T cells are primed after the acute phase of infection. These newly recruited T cells are phenotypically distinct from those primed earlier. Long-lived antiviral CD8 T cells are defective in self-renewal, and lack of thymic output results in the decline of virus-specific CD8 T cells, indicating that newly generated T cells preserve antiviral CD8 T cell populations during chronic infection. These findings reveal a novel role for antigen in maintaining virus-specific CD8 T cells during persistent infection and provide insight toward understanding T cell differentiation in chronic infection.
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