Linked Life Data

16189661

Source:http://linkedlifedata.com/resource/pubmed/id/16189661

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-3-1
pubmed:abstractText
The current study investigated the effect of tetrachlorodibenzo-p-dioxin (TCDD) on the ability of staphylococcal enterotoxin A (SEA)-primed T cells to divide by dual-labeling the cells with 5,6-carboxyfluorescein diacetate succinimidyl ester (CFSE) and antibodies against the specific T cell receptors. C57BL/6 wild-type mice were injected ip with TCDD (10 microg/kg body weight) followed by hind footpad injections of SEA (10 microg/footpad). The draining popliteal lymph nodes (PLN) were harvested 1-4 days posttreatment, labeled with CFSE and cultured for 1-4 days without further stimulation or in the presence of the recall antigen. TCDD-exposed SEA-reactive Vbeta3+ and Vbeta11+ T cells showed decreased cell divisions upon in vitro culture in the absence of any stimulation, which correlated with increased levels of apoptosis. The recall cell-division response was also defective in SEA-reactive T cells isolated from TCDD-exposed mice. However, during the recall response, cells from TCDD-exposed mice did not exhibit a defect in apoptosis, suggesting the defective recall response may result from a state of anergy rather than increased apoptosis. Using AhR knockout (KO) mice, we found AhR involvement in the regulation of defective cell division and apoptosis induced by TCDD. Together, these data demonstrate, while TCDD-induced apoptosis may account for the decreased primary T cell proliferative response, that the reduced cell division seen during subsequent exposure to recall antigen may result from a state of anergy. The study also demonstrates that a combined use of superantigen and CFSE may offer a simple and useful tool to monitor the ability of immunotoxicants to alter the proliferative responsiveness of antigen-specific T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0340-5761
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
134-45
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16189661-Animals, pubmed-meshheading:16189661-Apoptosis, pubmed-meshheading:16189661-Cell Division, pubmed-meshheading:16189661-Cell Survival, pubmed-meshheading:16189661-Dose-Response Relationship, Drug, pubmed-meshheading:16189661-Enterotoxins, pubmed-meshheading:16189661-Environmental Pollutants, pubmed-meshheading:16189661-Female, pubmed-meshheading:16189661-Fluoresceins, pubmed-meshheading:16189661-Fluorescent Dyes, pubmed-meshheading:16189661-Lymphocyte Activation, pubmed-meshheading:16189661-Mice, pubmed-meshheading:16189661-Mice, Inbred C57BL, pubmed-meshheading:16189661-Mice, Knockout, pubmed-meshheading:16189661-Staphylococcus aureus, pubmed-meshheading:16189661-Succinimides, pubmed-meshheading:16189661-Superantigens, pubmed-meshheading:16189661-T-Lymphocytes, pubmed-meshheading:16189661-Tetrachlorodibenzodioxin
pubmed:year
2006
pubmed:articleTitle
Superantigen-primed T cells exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) replicate poorly following recall encounter.
pubmed:affiliation
Department of Microbiology and Immunology, Medical College of Virginia Campus, Virginia Commonwealth University, 980613, Richmond, 23298, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural