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IL-2-Mediated Cell Cycle Progression and Inhibition of Apoptosis Does Not Require NF-B or Activating Protein-1 Activation in Primary Human T Cells¹

Department of Biology and Molecular Biology Institute, San Diego State University, San Diego, CA 92182 ⁵Abbreviations used in this paper: AP-1, activating protein-1; JNK, Jun N-terminal kinase; TBC, thymic blast cell; PB, peripheral blood; EMSA, electrophoretic mobility shift assay; TPA, o-tetradecanoylphorbol 13-acetate; TRE, TPA response element; TUNEL, terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling.

The IL-2 growth hormone is the major growth factor of activated T lymphocytes during a developing immune response. IL-2 is required not only for cell cycle progression but also to protect Ag-activated T cells from programmed cell death. In several cell types, activation of NF-B and/or activating protein-1 (AP-1) has been demonstrated to be extremely important in blocking apoptosis. To determine whether either or both of these transcription factors are involved in cell survival or cell cycle progression in response to IL-2, primary human T cells responsive to the growth factor were analyzed for NF-B and AP-1 activation. The current study clearly demonstrates that IL-2 does not induce IB degradation or NF-B activation in primary human T cells that respond to IL-2 by entering the cell cycle and avoiding apoptosis. Similarly, IL-2 neither activates JNK nor increases AP-1 binding activity to a consensus o-tetradecanoylphorbol 13-acetate (TPA) response element. On the other hand, the growth factor does induce the activation of STAT3 and STAT5 in these cells, as has been previously demonstrated. These data show that neither NF-B nor AP-1 activation is required for IL-2-mediated survival or cell cycle progression in activated primary human T cells.

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