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Program in Immunology, Department of Pathology, Tufts University School of Medicine, Boston, MA 02111;
Howard Hughes Medical Institute and Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19704;
Department of Pathology, School of Medicine, University of New Mexico, Albuquerque, NM 87131; and
§
Trudeau Institute, Saranac Lake, NY 12983
Th1- and Th2-type cells mediate distinct effector functions via
cytokine secretion in response to immunologic challenge. Precursor Th
cells transcribe IFN-
, IL-2, and IL-4 upon activation. Repeated
stimulation of Th precursor cells in the presence of IL-4 leads to
terminally differentiated Th2 cells that have lost the ability to
transcribe the IL-2 gene. We provide evidence that repression of IL-2
gene expression in Th2 cells and partial repression in Th1 cells are
mediated by ZEB, a zinc finger, E box-binding transcription factor.
This factor binds to a negative regulatory element, NRE-A, in the IL-2
promoter, thereby acting as a potent repressor of IL-2 transcription.
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