Superantigen-primed T cells exposed to 2,3,7,8–tetrachlorodibenzo-p-dioxin (TCDD) replicate poorly following recall encounter

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• 作者：Laura Faulconer (1)
  Iris Camacho (1)
  Mitzi Nagarkatti (1)
  Prakash S. Nagarkatti (2)
  
• 关键词：TCDD ; Immunosuppression ; CFSE
• 刊名：Archives of Toxicology
• 出版年：2006
• 出版时间：March 2006
• 年：2006
• 卷：80
• 期：3
• 页码：134-145
• 全文大小：685KB
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  2. Camacho IA, Nagarkatti M, Nagarkatti PS (2002) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces Fas-dependent activation-induced cell death in superantigen-primed T cells. Arch Toxicol 76:570-80 CrossRef
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• 作者单位：Laura Faulconer (1)
  Iris Camacho (1)
  Mitzi Nagarkatti (1)
  Prakash S. Nagarkatti (2)
  
  1. Department of Microbiology and Immunology, Medical College of Virginia Campus, Virginia Commonwealth University, 980613, Richmond, VA, 23298, USA
  2. Department of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, 980613, Richmond, VA, 23298, USA
  
• ISSN：1432-0738

文摘

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?μg/kg body weight) followed by hind footpad injections of SEA (10?μg/footpad). The draining popliteal lymph nodes (PLN) were harvested 1- days posttreatment, labeled with CFSE and cultured for 1- days without further stimulation or in the presence of the recall antigen. TCDD-exposed SEA-reactive Vβ3+ and Vβ11+ 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.