Linked Life Data

20720513

Source:http://linkedlifedata.com/resource/pubmed/id/20720513

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-2-18
pubmed:abstractText
Although it is known that injury enhances the regulatory activity of CD4 regulatory T cells (Tregs), the cellular and molecular mechanisms responsible for injury-induced Treg activation remain unclear. This study was designed to investigate and compare injury-induced T-cell receptor (TCR) signaling in Tregs, non-Tregs, and CD8 T cells. Specifically, we used phospho-flow cytometry to measure the expression and phosphorylation of ZAP-70, protein kinase C ?, nuclear factor of activated T cells, and glycogen synthase kinase 3? in FoxP3 Tregs versus FoxP3 non-Tregs versus CD8 T cells. Groups of male C57BL/6J mice underwent burn or sham injury, and lymph nodes and spleens were harvested at early time points-15, 30, 60, 120, and 240 min-to measure TCR signaling. As early as 15 min after burn injury, we observed a significant upregulation and phosphorylation of ZAP-70, protein kinase C ?, nuclear factor of activated T cells, and glycogen synthase kinase 3? in Tregs prepared from injury-site-draining lymph nodes. Burn injury did not activate TCR signaling in Tregs from the spleen or in CD4 non-Tregs and CD8 T cells. In conclusion, the results of this study demonstrate that burn injury activates TCR signaling in Tregs, but not non-Tregs or CD8 T cells. These findings suggest that injury provides an early TCR-activating signal to Tregs and supply new insights into how injury influences the adaptive immune system.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1540-0514
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
252-7
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Injury induces early activation of T-cell receptor signaling pathways in CD4+ regulatory T cells.
pubmed:affiliation
Department of Surgery (Immunology), Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural