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B Activation in Perforin Expression of NK Cells Upon IL-2 Receptor Signaling1
* Cancer Prevention and Research Center and Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, WA 99164; and
Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, FL 33101
Optimal NK cell development and activation as well as cytolytic
activity involves IL-2R
signals that also up-regulate expression of
the pore-forming effector molecule perforin. Although the Jak/Stat
pathway and specifically Stat5 transcription factors are required to
promote many of the respective downstream events, the role of
additional signaling pathways and transcription factors remains to be
clarified. This report investigates the role of NF-
B activation for
perforin expression by NK cells. It is demonstrated that IL-2-induced
up-regulation of perforin in primary NK cells and in a model cell line
is blocked by two pharmacological agents known to inhibit NF-B
activation. Direct evidence for the activation of the NF-B pathway
by IL-2R signals in NK cells involves activation of the IKK
kinase,
inhibitory protein B degradation, nuclear translocation of
p50/p65 complexes, and ultimately, transcriptional activation of the
perforin gene via an NF-B binding element in its upstream enhancer.
Taken together, these observations strongly suggest that IL-2R signals
can activate a pathway leading to NF-B activation in NK cells and
that this pathway is involved in the control of perforin
expression.
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