Reciprocal Activating Interaction between Natural Killer Cells and Dendritic Cells
By F. Gerosa, Barbara Baldani-Guerra, C. Nisii, Viviana Marchesini, G. Carra, G. Trinchieri. Journal of Experimental Medicine, 2002
1,163 citations recorded by the source corpus.
We analyzed the interaction between human peripheral blood natural killer (NK) cells and monocyte-derived immature dendritic cells (DC). Fresh NK cells were activated, as indicated by the induced expression of the CD69 antigen, and their cytolytic activity was strongly augmented by contact with lipopolysaccharide (LPS)-treated mature DC, or with immature DC in the presence of the maturation stimuli LPS, Mycobacterium tuberculosis or interferon (IFN)-α. Reciprocally, fresh NK cells cultured with immature DC in the presence of the maturation stimuli strongly enhanced DC maturation and interleukin (IL)-12 production. IL-2–activated NK cells directly induced maturation of DC and enhanced their ability to stimulate allogeneic naive CD4+ T cells. The effects of NK cells were cell contact dependent, although the secretion of IFN-γ and TNF also contributed to DC maturation. Within peripheral blood lymphocytes the reciprocal activating interaction with DC was restricted to NK cells, because the other lymphocyte subsets were neither induced to express CD69, nor induced to mature in contact with DC. These data demonstrated for the first time a bidirectional cross talk between NK cells and DC, in which NK cells activated by IL-2 or by mature DC induce DC maturation.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/a1b7bfc3689563d8f64c3596509ca841ed1e19a4
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Citations in the corpus
- Dendritic cells prime natural killer cells by trans-presenting interleukin 15. (2007, background): “…from in vitro coculture experiments employing TLR-stimulated or infected BM- or monocyte-derived DCs or macrophages (Andoniou et al., 2005; Chambers et al., 1996; Ferlazzo et al., 2004; Fernandez et al., 1999; Gerosa et al., 2002; Jinushi et al., 2003a; Koka et al., 2004; Krug et al., 2004).”
- Natural selection of tumor variants in the generation of “tumor escape” phenotypes (2002, background): “In “sterile” environments, as seen with tumors or transplantation, such stimulatory factors may not be readily available, and the cross-talk between DCs and resting NK cells that induces NK cell activation may not occu”
- Interleukin-12 and the regulation of innate resistance and adaptive immunity (2003, background): “The secondary signals for IL-12 production might come not only from activated T cells in adaptive immunity, but also from effector cells of innate resistance, such as NK cells, both through secretion of IFN-γ and IL-13, and through cell–cell interaction”
- TNF/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection. (2003, background): “This monocyte subset ex- cells were shown to induce IFN- secretion by NK cells presses CCR2 and thus may represent a precursor of (Ferlazzo et al., 2002; Gerosa et al., 2002).”
- Cancer immunoediting: from immunosurveillance to tumor escape (2002, background): “In the draining lymph node, the newly immigrated dendritic cells induce tumor-specific CD4 + T helper cells expressing IFN-γ (T H 1 cells) that in turn facilitate the development of tumor-specific CD8 + T cell”
- Dendritic cells: translating innate to adaptive immunity. (2006, background): “NK cells are the prototype [10–12], but NKT cells [13, 14] and γδ T cells [15] might be included.”
- New aspects of natural-killer-cell surveillance and therapy of cancer (2002, background): “Priming of adaptive tumour immunity by NK cells It has recently become apparent that NK cells might also influence development of the adaptive immune response by interacting with DC”