Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-11-15
pubmed:abstractText
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.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1074-7613
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
515-25
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Sensory neurons regulate the effector functions of CD8+ T cells in controlling HSV-1 latency ex vivo.
pubmed:affiliation
Graduate Program in Immunology, University of Pittsburgh School of Medicine, 203 Lothrop Street, Pittsburgh, Pennsylvania 15213, USA.
pubmed:publicationType
Journal Article, Retracted Publication, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural