Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 3, Pages 1419-1428Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1001140
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Funding
- National Institutes of Health U.S. Public Health Service [AI-017672, AI-081675]
- National Institutes of Health [T32AIO7349-16]
- National Institutes of Health Diabetes and Endocrinology Center [DK32520]
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Nonvirus-specific bystander CD8 T cells bathe in an inflammatory environment during viral infections. To determine whether bystander CD8 T cells are affected by these environments, we examined P14, HY, and OT-I TCR transgenic CD8 T cells sensitized in vivo by IFN-alpha beta-inducing viral infections or by polyinosinic: polycytidylic acid. These sensitized cells rapidly exerted effector functions, such as IFN-gamma production and degranulation, on contact with their high-affinity cognate Ag. Sensitization required self-MHC I and indirect effects of IFN-alpha beta, which together upregulated the T-box transcription factor Eomesodermin, potentially enabling the T cells to rapidly transcribe CTL effector genes and behave like memory cells rather than naive T cells. IL-12, IL-15, IL-18, and IFN-gamma were not individually required for sensitization to produce IFN-gamma, but IL-15 was required for upregulation of granzyme B. These experiments indicate that naive CD8 T cells receive signals from self-MHC and IFN-alpha beta and that, by this process, CD8 T cell responses to viral infection can undergo distinct differentiation pathways, depending on the timing of Ag encounter during the virus-induced IFN response. The Journal of Immunology, 2010, 185: 1419-1428.
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