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Published online before print December 16, 2004
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,1
* Departments of Pathology and
Cell Biology and Physiology, University of Pittsburgh School of Medicine, and
University of Pittsburgh Cancer Institute, Pennsylvania
1 Correspondence: University of Pittsburgh Cancer Institute, Hillman Cancer Center, G.17d, 5117 Centre Avenue, Pittsburgh, PA 15213-1863. E-mail: vujanovicnl{at}msx.upmc.edu
Dendritic cells (DC) and natural killer (NK) cells are essential components of the innate immune system, which rapidly sense and eliminate invading pathogens and transformed cells, mediate inflammation, and initiate adaptive immune responses. During the early immune events, DC and NK cells interact and regulate each other. The cellular "cross talk" and its molecular mediators are believed to be critical to the quality and magnitude of innate and adaptive immune responses. The goal of the present manuscript is to identify and initially assess major molecular mediators of DC-NK cell interaction. We have previously shown that DC and NK cells constitutively express several tumor necrosis factor family ligands (TNFfLs) and corresponding TNF family receptors (TNFfRs). Therefore, DC and NK cells might be able to interact via cognate interplays of TNFfLs and TNFfRs. Here, we provide initial experimental evidence supporting this possibility. We found that combined but not individual ligation of several TNFfRs induced substantial increases in secretion of interleukin-12 and inteferon-
by DC and NK cells, respectively. In contrast, specific, individual disruptions of the engagements of the corresponding TNfL-TNFfR pairs greatly impaired DC and NK cell abilities to reciprocally mediate the increases in cytokine secretion. These findings indicate that multiple TNFfLs mediate DC-NK cell interaction.
Key Words: NK cells • interaction • TNF family ligands
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