Journal
IMMUNITY
Volume 23, Issue 5, Pages 515-525Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2005.09.017
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Funding
- NEI NIH HHS [P30EY08098, EY05945, EY015291] Funding Source: Medline
- NINDS NIH HHS [F30 NS50905-01] Funding Source: Medline
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We provide evidence that sensory neurons regulate the effector functions and phenotype of CD8(+) T cells during active immunosurveillance of HSV-1 latency. Low-level viral gene expression in latently infected sensory ganglia gives rise to a unique, functionally active CD8(+) T cell population. Surprisingly, distinct neuronal subsets require different CD8 effector mechanisms to maintain viral latency, with some requiring IFN-gamma and others requiring lytic granules (LG). This nonredundant efficacy of CD8(+) T cell effector mechanisms in maintaining viral latency is explained as follows: (1) a subset of neurons that expresses IFN-gamma receptors (IFN-gamma R+) and Qa1 responds to IFN-gamma, but Qa1 engagement of CD94/NKG2a blocks LG exocytosis by CD8(+) T cells; (2) another neuronal subset is responsive to LG because it lacks Gal and is refractory to IFN-gamma because it also lacks IFN-gamma R. In the latter subset, LG appear to provide a nonlethal block of viral reactivation.
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