Source:http://linkedlifedata.com/resource/pubmed/id/16785503
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2006-6-20
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| pubmed:abstractText |
Overwhelming infection remains the leading cause of death from serious burn injury despite recent advances in the care of burn patients and a better understanding of immune and inflammatory consequences of injury. In this study, we report a critical requirement for CD1d-restricted NKT cells and CD1d expression by APCs in the immune dysfunction that occurs early after burn injury. Using a well-established murine scald injury model with BALB/c and BALB/c CD1d knockout mice, we investigated whether peripheral T cell immunity was affected by the presence or absence of CD1d-restricted NKT cells in the early stages after injury. Using Ag-specific delayed-type hypersensitivity, T cell proliferation, and cytokine production as indices of immune responsiveness, we observed that both CD1d expression by APCs and CD1d-restricted NKT cells are required for immune suppression after injury. Via adoptive transfer of splenocytes from injured mice to uninjured recipients, we found injury-induced suppression of immunity to be Ag specific, long lasting, and critically dependent on cell surface expression of CD1d by APCs. Together, our results suggest that the defects in T cell responsiveness that occur subsequent to severe burn injury are not merely the result of global or passive suppression, but instead represent an active form of CD1d/NKT cell-dependent immunologic tolerance.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
177
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
92-9
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16785503-Adoptive Transfer,
pubmed-meshheading:16785503-Animals,
pubmed-meshheading:16785503-Antigen-Presenting Cells,
pubmed-meshheading:16785503-Antigens, CD1,
pubmed-meshheading:16785503-Antigens, CD1d,
pubmed-meshheading:16785503-Burns,
pubmed-meshheading:16785503-Cells, Cultured,
pubmed-meshheading:16785503-Genetic Predisposition to Disease,
pubmed-meshheading:16785503-Immune Tolerance,
pubmed-meshheading:16785503-Immunity, Cellular,
pubmed-meshheading:16785503-Interferon-gamma,
pubmed-meshheading:16785503-Interleukin-4,
pubmed-meshheading:16785503-Killer Cells, Natural,
pubmed-meshheading:16785503-Male,
pubmed-meshheading:16785503-Mice,
pubmed-meshheading:16785503-Mice, Inbred BALB C,
pubmed-meshheading:16785503-Mice, Knockout,
pubmed-meshheading:16785503-Spleen,
pubmed-meshheading:16785503-T-Lymphocyte Subsets
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Injury-induced suppression of effector T cell immunity requires CD1d-positive APCs and CD1d-restricted NKT cells.
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| pubmed:affiliation |
Department of Surgery, and Burn and Shock Trauma Institute, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|