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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1998-7-16
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pubmed:abstractText |
Numerous reports have demonstrated a link between stressful stimuli and immune suppression. However, the cellular mechanisms by which stress impairs immune function are largely unknown. We have examined the effects of an acute stressor on the T cell population, specifically, the number and phenotype of T cells in a nonhuman primate model. In nonstressed adult monkeys, we found differences in the level of expression of CD2 on T cells, revealing two distinct subsets of T cells, CD2dim and CD2bright cells, with CD2bright cells predominately coexpressing CD8. In response to acute stress, we observed a significant loss in the number and percent of CD2bright/CD8+ cells, with percent of CD2bright cells returning to pre-stress values within 24 h.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0165-5728
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
86
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
63-73
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:9655473-Acute Disease,
pubmed-meshheading:9655473-Animals,
pubmed-meshheading:9655473-Antigens, CD2,
pubmed-meshheading:9655473-CD4-Positive T-Lymphocytes,
pubmed-meshheading:9655473-CD8-Positive T-Lymphocytes,
pubmed-meshheading:9655473-Cell Adhesion Molecules,
pubmed-meshheading:9655473-Female,
pubmed-meshheading:9655473-Flow Cytometry,
pubmed-meshheading:9655473-Macaca fascicularis,
pubmed-meshheading:9655473-Stress, Physiological
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pubmed:year |
1998
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pubmed:articleTitle |
Selective reduction in CD2 expression on CD2bright/CD8+ lymphocytes from cynomolgus monkeys (Macaca fascicularis) in response to acute stress.
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pubmed:affiliation |
Department of Cell Biology and Physiology, University of Pittsburgh, PA 15261, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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