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The Journal of Immunology, Vol 145, Issue 10 3340-3347, Copyright © 1990 by American Association of Immunologists
ARTICLES |
G Plaetinck, MC Combe, P Corthesy, P Sperisen, H Kanamori, T Honjo and M Nabholz
Swiss Institute for Experimental Cancer Research, Genetics Unit, Epalinges, Switzerland.
We have analyzed the mechanisms by which IL-1, IL-2, and TNF regulate expression of IL-2R alpha chain in a rodent T cell line. All three cytokines induce detectable IL-2R alpha mRNA by themselves, but there is strong synergy between IL-1 or TNF, on the one hand, and IL-2, on the other. The earliest phase of induction by IL-1 is independent of protein synthesis. IL-1, but not TNF, also stimulates transient secretion of IL-2. This leads to an autocrine stimulation of a further increase in IL-2R alpha mRNA levels. When IL-2 secretion has dropped off, continued IL-2R alpha expression requires both IL-2 and IL-1. Most or all of this regulation is due to changes in the rate of transcription of the IL-2R alpha gene. The response to IL-1 and IL-2 depends on a segment in the IL-2R alpha 5' flanking region, upstream of all cis-acting regulatory elements previously identified in the human gene.
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