Skip Navigation


ToxSci Advance Access originally published online on February 19, 2004
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
79/1/98    most recent
kfh090v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (2)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Brundage, K. M.
Right arrow Articles by Barnett, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brundage, K. M.
Right arrow Articles by Barnett, J. B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Toxicological Sciences 79, 98-105 (2004)
Toxicological Sciences vol. 79 no. 1 © Society of Toxicology; all rights reserved.

Altered AP-1 (Activating Protein-1) Activity and c-jun Activation in T Cells Exposed to the Amide Class Herbicide 3,4-Dichloropropionanilide (DCPA)

K. M. Brundage, R. Schafer and J. B. Barnett1

Department of Microbiology, Immunology and Cell Biology, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, West Virginia 26506–9177

Received October 15, 2003; accepted January 24, 2004

3,4-Dichloropropionanilide (DCPA), the active ingredient of some postemergence herbicides, has been demonstrated to inhibit several immune system functions including cytokine production by T cells. The central role of cytokines in regulating the immune response suggests a possible mechanism by which DCPA inhibits the immune system. Since interleukin (IL)-2 is critical in regulating many immune functions, we chose to investigate the effect of DCPA on this cytokine. Using the human T lymphoma line, Jurkat, stimulated with phorbol-12-myristate acetate (PMA) and the calcium ionophore A23187 (Io), we determined that DCPA exposure decreased IL-2 secretion and mRNA levels in a dose dependent manner. We hypothesized that DCPA affected one or more of the transcription factors that regulate IL-2 gene transcription. Activating protein 1(AP-1) is a transcription factor that has been demonstrated to be required for optimal IL-2 gene transcription. Electrophoretic mobility shift assays (EMSAs) demonstrated a decreased level of AP-1 DNA binding activity in DCPA-exposed Jurkat cells compared to control cells from 30 min to 2 h after stimulation. The altered AP-1 DNA binding kinetics was associated with a decrease in c-jun protein in these cells at 1 and 2 h after exposure and a decreased level of phosphorylated c-jun at 1–4 h after exposure. These results suggest a possible mechanism for DCPA-induced IL-2 inhibition; alteration in the activation of the c-jun component of AP-1.

Key Words: 3,4-dichloropropionanilide; AP-1; c-jun; IL-2; T cell; propanil.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Toxicol SciHome page
T. L. Lewis, K. M. Brundage, R. A. Brundage, and J. B. Barnett
3,4-Dichloropropionanilide (DCPA) Inhibits T-Cell Activation by Altering the Intracellular Calcium Concentration following Store Depletion
Toxicol. Sci., May 1, 2008; 103(1): 97 - 107.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.