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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Sensory neurons regulate the effector functions of CD8(+) T cells in controlling HSV-1 latency ex vivo.

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 Qa 1 responds to IFN-gamma, but Qa 1 engagement of CD94/NKG2a blocks LG exocytosis by CD8(+) T cells; (2) another neuronal subset is responsive to LG because it lacks Qa 1 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.[1]

References

  1. Sensory neurons regulate the effector functions of CD8(+) T cells in controlling HSV-1 latency ex vivo. Prabhakaran, K., Sheridan, B.S., Kinchington, P.R., Khanna, K.M., Decman, V., Lathrop, K., Hendricks, R.L. Immunity (2005) [Pubmed]
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