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J. Biol. Chem., Vol. 276, Issue 24, 21984-21989, June 15, 2001

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Interdependence of cdk2 Activation and Interleukin-2R Accumulation in T Cells^*

Subhra Mohapatra^§ and W. J. Pledger^§¶

From the  Molecular Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, ^§ Department of Oncology, and Department of Biochemistry and Molecular Biology, University of South Florida College of Medicine, Tampa, Florida 33612

We have shown previously that serum promotes T cell proliferation by acting with T cell receptor (TCR) agonists to efficiently down-regulate p27^Kip1 and activate cdk2-containing complexes. In the studies described here, the effect of serum on the expression of the  subunit of the interleukin-2 receptor (IL-2R) was examined. We found that serum was required for maximal and sustained IL-2R protein expression and consequent IL-2 signaling in TCR-activated splenocytes. Serum had no effect on IL-2R mRNA levels and thus modulates IL-2R expression post-transcriptionally. Unlike wild-type splenocytes, splenocytes exhibiting serum-independent cdk2 activation due to loss of p27^Kip1 efficiently expressed IL-2R in serum-deficient medium. Conversely, serum did not promote IL-2R accumulation in conditions in which cdk2 activity was blocked. These findings demonstrate that cdk2 activation is necessary and sufficient for IL-2R accumulation in TCR-stimulated splenocytes. On the other hand, IL-2 signaling was required (at least in part) for cdk2 activation in these cells. Thus, cdk2 activation, IL-2R expression, and IL-2 signaling are interdependent events, and we suggest that this feed-forward regulatory loop plays a key role in T cell mitogenesis.

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