Linked Life Data

19729482

Source:http://linkedlifedata.com/resource/pubmed/id/19729482

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-10-7
pubmed:abstractText
Reduced immune function is frequently a consequence of serious injury such as trauma-hemorrhage (T-H). Injury may lead to reduced T-cell activation, resulting in decreased engagement of costimulatory molecules after antigen recognition and in subsequent immunological compromise and anergy. We hypothesized that inhibition of CD28 expression is one possible mechanism by which immune functions are suppressed after T-H. Male C3H/HeN mice (with or without ovalbumin immunization) were subjected to sham operation or T-H and sacrificed after 24 hours. Splenic T cells were then stimulated with concanavalin A or ovalbumin in vivo or in vitro, and CD28, cytotoxic T-lymphocyte antigen 4 (CTLA-4), CD69, and phospho-Akt expression was determined. T-cell proliferation/cytokine production was measured in vitro. Stimulation-induced CD69, CD28, and phospho-Akt up-regulation were significantly impaired after T-H compared with sham-operated animals; however, CTLA-4 expression was significantly higher in the T-H group. Over a 3-day span, stimulated T cells from sham-operated animals showed significantly higher proliferation compared with the T-H group. IL-2 and IFN-gamma were elevated in sham-operated animals, whereas IL-4 and IL-5 rose in the T-H group, revealing a shift from T(H)1 to T(H)2 type cytokine production after T-H. Dysregulation of the T-cell costimulatory pathway is therefore likely to be a significant contributor to post-traumatic immune suppression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1525-2191
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
175
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1504-14
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:19729482-Animals, pubmed-meshheading:19729482-Antigens, CD, pubmed-meshheading:19729482-Antigens, CD28, pubmed-meshheading:19729482-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:19729482-CD4-Positive T-Lymphocytes, pubmed-meshheading:19729482-CTLA-4 Antigen, pubmed-meshheading:19729482-Cell Proliferation, pubmed-meshheading:19729482-Cells, Cultured, pubmed-meshheading:19729482-Concanavalin A, pubmed-meshheading:19729482-Cytokines, pubmed-meshheading:19729482-Enzyme Activation, pubmed-meshheading:19729482-Hemorrhage, pubmed-meshheading:19729482-Immune Tolerance, pubmed-meshheading:19729482-Lectins, C-Type, pubmed-meshheading:19729482-Lymphocyte Activation, pubmed-meshheading:19729482-Mice, pubmed-meshheading:19729482-Ovalbumin, pubmed-meshheading:19729482-Proto-Oncogene Proteins c-akt, pubmed-meshheading:19729482-Signal Transduction, pubmed-meshheading:19729482-Spleen, pubmed-meshheading:19729482-Wounds and Injuries
pubmed:year
2009
pubmed:articleTitle
Suppression of activation and costimulatory signaling in splenic CD4+ T cells after trauma-hemorrhage reduces T-cell function: a mechanism of post-traumatic immune suppression.
pubmed:affiliation
Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35294-0019, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural