Coumestrol, Bisphenol-A, DDT, and TCDD Modulation of Interleukin-2 Expression in Activated CD+4 Jurkat T Cells

International Journal of Environmental Research and Public Health

Kenneth Ndebele¹  Paul B. Tchounwou¹ 

[1] ¹Molecular Toxicology Research Laboratory, NIH- Center for Environmental Health, School of Science and Technology, Jackson State University, 1400 Lynch Street, P.O. Box 18540, Jackson, Mississippi, USA ²Rheumatology Section, G.V. (Sonny) Montgomery V.A. Hospital and Division of Rheumatology and Molecular Immunology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA

关键词: Xenoestrogens;    IL-2;    transcription;    Jurkat T cells;   

DOI  :  10.3390/ijerph2004010003

来源: mdpi

【 摘 要 】

Endogenous estrogens are known to modulate several components of immune response, including interleukin-2 (IL-2) production. IL-2 is a cytokine that plays an important role in adaptive immune responses. These responses may be modulated by xenoestrogens such as coumestrol, bisphenol A (BPA), DDT, and TCDD. In this research, we examined the effects and potential mechanisms of action of these estrogenic compounds on IL-2 production in activated CD4+ Jurkat T cells. IL-2 production was analyzed by ELISA and Western Blot. At the transcriptional level, protein expression was examined by RT-PCR. Coumestrol, DDT and TCDD (but not BPA) significantly suppressed IL-2 production in activated CD4+ Jurkat T cells, at the transcriptional and translational levels. The transcriptional suppression of IL-2 was associated with decreased protein levels of NF-κβ, an important IL-2 positive transcription factor, without affecting the expression of Iκ−Βα protein expression, an important inhibitor of NF-κβ nuclear translocation. Although the direct mechanisms of xenoestrogens modulation of the immune system remain to be elucidated, coumestrol-, DDT- and TCDD-induced suppression of IL-2 may have ramifications for our understanding of the impact of xenoestrogens on health and disease.

【 授权许可】

CC BY   
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.