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Nuclear Pro-IL-16 Regulation of T Cell Proliferation: p27^KIP1-Dependent G₀/G₁ Arrest Mediated by Inhibition of Skp2 Transcription¹

The Pulmonary Center, Boston University School of Medicine, Boston, MA 02118

The precursor for IL-16 (pro-IL-16) is a nuclear and cytoplasmic PDZ domain-containing protein. In this study we have found that pro-IL-16 is absent or mutated in four T lymphoblastic leukemia cell lines examined. Ectopic expression of pro-IL-16 in pro-IL-16-negative Jurkat cells blocks cell cycle progression from G₀/G₁ to S phase associated with elevated levels of the cyclin-dependent kinase inhibitor p27^KIP1. Pro-IL-16 decreases p27^KIP1 degradation by reducing transcription and subsequent expression of Skp2, a key component of the SCF^Skp2 ubiquitin E3 ligase complex. Taken together, these findings identify pro-IL-16 as a novel regulator of Skp2 expression and p27^KIP1 levels and implicate a role for pro-IL-16 in T cell proliferation.

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