| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
Published online before print December 16, 2004
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Article |
,,,,,
,@
Departments of *Pathology and Cell Biology and Physiology, University of Pittsburgh School of Medicine, and University of Pittsburgh Cancer Institute, Pennsylvania
@ To whom correspondence should be addressed. E-mail: vujanovicnl{at}msx.upmc.edu.
 |
Abstract |
|---|
Dendritic cells (DC) and natural killer (NK) cells are essential components of the innate immune system, which rapidly senses and eliminates invading pathogens and transformed cells, mediates inflammation, and initiates 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
This article has been cited by other articles:
|
|
 |
|
  R. Winkler-Pickett, H. A. Young, J. M. Cherry, J. Diehl, J. Wine, T. Back, W. E. Bere, A. T. Mason, and J. R. Ortaldo In Vivo Regulation of Experimental Autoimmune Encephalomyelitis by NK Cells: Alteration of Primary Adaptive Responses J. Immunol., April 1, 2008; 180(7): 4495 - 4506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Tian, S. Grimaldo, M. Fugita, J. Cutts, N. L. Vujanovic, and L.-Y. Li The Endothelial Cell-Produced Antiangiogenic Cytokine Vascular Endothelial Growth Inhibitor Induces Dendritic Cell Maturation J. Immunol., September 15, 2007; 179(6): 3742 - 3751. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Xu, A. K. Chakrabarti, J. L. Tan, L. Ge, A. Gambotto, and N. L. Vujanovic Essential role of the TNF-TNFR2 cognate interaction in mouse dendritic cell-natural killer cell crosstalk Blood, April 15, 2007; 109(8): 3333 - 3341. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Huang, M. Kucia, F. Rezzoug, J. Ratajczak, M. K. Tanner, M. Z. Ratajczak, C. L. Schanie, H. Xu, I. Fugier-Vivier, and S. T. Ildstad Flt3-Ligand-Mobilized Peripheral Blood, but Not Flt3-Ligand-Expanded Bone Marrow, Facilitating Cells Promote Establishment of Chimerism and Tolerance Stem Cells, April 1, 2006; 24(4): 936 - 948. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
