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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2005-2-24
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pubmed:abstractText |
Major injury initiates a systemic inflammatory response that can be detrimental to the host. We have recently reported that burn injury primes innate immune cells for a progressive increase in TLR4 and TLR2 agonist-induced proinflammatory cytokine production and that this inflammatory phenotype is exaggerated in adaptive immune system-deficient (Rag1(-/-)) mice. The present study uses a series of adoptive transfer experiments to determine which adaptive immune cell type(s) has the capacity to control innate inflammatory responses after injury. We first compared the relative changes in TLR4- and TLR2-induced TNF-alpha, IL-1beta, and IL-6 production by spleen cell populations prepared from wild-type (WT), Rag1(-/-), CD4(-/-), or CD8(-/-) mice 7 days after sham or burn injury. Our findings indicated that splenocytes prepared from burn-injured CD8(-/-) mice displayed TLR-induced cytokine production levels similar to those in WT mice. In contrast, spleen cells from burn-injured CD4(-/-) mice produced cytokines at significantly higher levels, equivalent to those in Rag1(-/-) mice. Moreover, reconstitution of Rag1(-/-) or CD4(-/-) mice with WT CD4(+) T cells reduced postinjury cytokine production to WT levels. Additional separation of CD4(+) T cells into CD4(+)CD25(+) and CD4(+)CD25(-) subpopulations before their adoptive transfer into Rag1(-/-) mice showed that CD4(+)CD25(+) T cells were capable of reducing TLR-stimulated cytokine production levels to WT levels, whereas CD4(+)CD25(-) T cells had no regulatory effect. These findings suggest a previously unsuspected role for CD4(+)CD25(+) T regulatory cells in controlling host inflammatory responses after injury.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidoglycan,
http://linkedlifedata.com/resource/pubmed/chemical/RAG-1 protein,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tlr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tlr4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2957-63
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15728508-Adoptive Transfer,
pubmed-meshheading:15728508-Animals,
pubmed-meshheading:15728508-Antigens, CD4,
pubmed-meshheading:15728508-Burns,
pubmed-meshheading:15728508-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15728508-Homeodomain Proteins,
pubmed-meshheading:15728508-Immunity, Innate,
pubmed-meshheading:15728508-Inflammation Mediators,
pubmed-meshheading:15728508-Interleukin-1,
pubmed-meshheading:15728508-Interleukin-6,
pubmed-meshheading:15728508-Lipopolysaccharides,
pubmed-meshheading:15728508-Male,
pubmed-meshheading:15728508-Mice,
pubmed-meshheading:15728508-Mice, Inbred C57BL,
pubmed-meshheading:15728508-Mice, Knockout,
pubmed-meshheading:15728508-Peptidoglycan,
pubmed-meshheading:15728508-Receptors, Cell Surface,
pubmed-meshheading:15728508-Receptors, Interleukin-2,
pubmed-meshheading:15728508-Spleen,
pubmed-meshheading:15728508-T-Lymphocytes, Regulatory,
pubmed-meshheading:15728508-Toll-Like Receptor 2,
pubmed-meshheading:15728508-Toll-Like Receptor 4,
pubmed-meshheading:15728508-Tumor Necrosis Factor-alpha
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pubmed:year |
2005
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pubmed:articleTitle |
CD4+CD25+ regulatory T cells control innate immune reactivity after injury.
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pubmed:affiliation |
Department of Surgery (Immunology), Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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