Modulation of Lymphocyte IL-2 Expression and Apoptosis by Estrogenic Xenobiotics

EPA Grant Number: U915917
Title: Modulation of Lymphocyte IL-2 Expression and Apoptosis by Estrogenic Xenobiotics
Investigators: Ndebele, Kenneth
Institution: Jackson State University
EPA Project Officer: Graham, Karen
Project Period: January 1, 2001 through January 1, 2004
Project Amount: $104,062
RFA: Minority Academic Institutions (MAI) Fellowships for Graduate Environmental Study (2001) RFA Text |  Recipients Lists
Research Category: Ecological Indicators/Assessment/Restoration , Academic Fellowships , Fellowship - Environmental Science


The objective of this research project is to show that estrogen suppresses interleukin-2 (IL-2) production from activated peripheral blood T cells and CD4+ T cell lines at the transcriptional level.


IL-2 plays an important role in adaptive immune responses. These responses differ between females and males; this may be because of the sex steroid estrogen. In CD4+ Jurkat T cells, transcriptional suppression of IL-2 was associated with decreased nuclear binding of two important IL-2 positive transcriptional binding factors, NFKbeta and AP-1. The decreased nuclear binding of NFKbeta occurred in the setting of estrogen-induced increases in IK–Ba protein levels, an important inhibitor of NFKbeta nuclear translocation. Moreover, estrogen also was shown to inhibit IL-2 receptor (IL2-R) expression in activated peripheral blood T cells. Estrogen-induced suppression of IL-2 and its receptor may have many ramifications for our understanding of immune and autoimmune sexual dichotomies, immune responses during pregnancy, and potential therapeutic intervention with hormone agonists and antagonists.

Supplemental Keywords:

fellowship, lymphocyte IL-2, lymphocyte IL-2 expression, apoptosis, estrogenic xenobiotics, immune responses, estrogen, sex steroid, peripheral blood T cells, estrogen-induced increases, nuclear translocation.

Progress and Final Reports:

  • 2001
  • 2002
  • Final