Linked Life Data

11551431

Source:http://linkedlifedata.com/resource/pubmed/id/11551431

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-9-11
pubmed:abstractText
T cells upon activation undergo apoptosis, a process termed activation-induced cell death (AICD). In the current study, we investigated whether 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases AICD and whether this constitutes one of the mechanisms by which TCDD induces immunotoxicity. To this end, C57BL/6+/+, C57BL/6 gld/gld (Fas ligand-defective) and C57BL/6 lpr/lpr (Fas-deficient) mice were injected with TCDD (50 microg/kg body weight, ip) or the vehicle (corn oil) and with anti-CD3 mAbs into the footpads. 3 days later, inguinal and popliteal lymph node cells were harvested, pooled and enumerated. Cells were cultured in vitro with anti-CD3 mAbs and cell proliferation was measured. Also, such cells were studied for their ability to undergo apoptosis upon in vitro culture with either tissue culture medium alone or with anti-CD3 mAbs. The data demonstrated that lymph nodes from TCDD-treated wild-type (+/+) mice showed a decrease in cellularity and the T cells exhibited decreased responsiveness to anti-CD3 mAbs when compared to the vehicle-treated control group. Furthermore, such cells from TCDD-treated mice exhibited increased levels of apoptosis upon in vitro culture when compared to the cells from vehicle-treated mice. In contrast, activated lymph nodes from TCDD-treated C57BL/6 gld/gld and C57BL/6 lpr/lpr mice showed normal cellularity and T cell responsiveness to anti-CD3 stimulation when compared to the vehicle controls. In addition, the activated lymph node T cells from the TCDD-treated C57BL/6 gld/gld and C57BL/6 lpr/lpr mice failed to exhibit increased apoptosis when compared to the controls. The current study demonstrates that the immunotoxic effects of TCDD in activated peripheral T cells may result from increased AICD mediated through Fas-Fas ligand interactions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0300-483X
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
51-63
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11551431-Animals, pubmed-meshheading:11551431-Antibodies, Monoclonal, pubmed-meshheading:11551431-Antigens, CD3, pubmed-meshheading:11551431-Antigens, CD95, pubmed-meshheading:11551431-Apoptosis, pubmed-meshheading:11551431-Cell Death, pubmed-meshheading:11551431-Cell Division, pubmed-meshheading:11551431-Environmental Pollutants, pubmed-meshheading:11551431-Female, pubmed-meshheading:11551431-Immunity, Cellular, pubmed-meshheading:11551431-In Situ Nick-End Labeling, pubmed-meshheading:11551431-Lymphocyte Activation, pubmed-meshheading:11551431-Mice, pubmed-meshheading:11551431-Mice, Inbred C57BL, pubmed-meshheading:11551431-RNA, Messenger, pubmed-meshheading:11551431-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11551431-T-Lymphocytes, pubmed-meshheading:11551431-Tetrachlorodibenzodioxin, pubmed-meshheading:11551431-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Enhanced activation-induced cell death as a mechanism of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced immunotoxicity in peripheral T cells.
pubmed:affiliation
Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0678, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't