The trafficking of natural killer cells

Grégoire, Claude; Chasson, Lionel; Luci, Carmelo; Tomasello, Elena; Geissmann, Frédéric; Vivier, Éric; Walzer, Thierry

doi:10.1111/j.1600-065x.2007.00563.x

Cited by 472 publications

(470 citation statements)

References 115 publications

(137 reference statements)

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“…Blocking of CXCR3 did not affect NK-cell migration to IFN-g/FMKp-matured DC; therefore, our data suggest that CXCR3-and CCR5-dependent NK-cell recruitments are two different mechanisms by which NK cells can be attracted by DC. Both chemokine receptors CXCR3 and CCR5 are expressed by subpopulations of resting and activated NK cells and have been proven essential for NK-cell migration to various tissues in response to proinflammatory stimuli [23,26,32]. Which NK-cell-recruitment mechanism is utilized seems to depend on the agents used in DC maturation and lack of NKcell recruitment by TNF-a/PGE2-matured DC suggests that TLR ligands or other PRR-triggering agents are necessary triggers for DC to recruit NK cells.…”

Section: Discussionmentioning

confidence: 99%

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Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells

et al. 2010

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Besides their role in destruction of altered self-cells, NK cells have been shown to potentiate T-cell responses by interacting with DC. To take advantage of NK-DC crosstalk in therapeutic DC-based vaccination for infectious diseases and cancer, it is essential to understand the biology of this crosstalk. We aimed to elucidate the in vitro mechanisms responsible for NK-cell recruitment and activation by DC during infection. To mimic bacterial infection, DC were exposed to a membrane fraction of Klebsiella pneumoniae, which triggers TLR2/4. DC matured with these bacterial fragments can actively recruit NK cells in a CCR5-dependent manner. An additional mechanism of DC-induced NK-cell recruitment is characterized by the induction of CCR7 expression on CD56 dim CD16 1 NK cells after physical contact with membrane fraction of K. pneumoniae-matured DC, resulting in an enhanced migratory responsiveness to the lymph node-associated chemokine CCL19. Bacterial fragment-matured DC do not only mediate NK-cell migration but also meet the prerequisites needed for augmentation of NK-cell cytotoxicity and IFN-c production, the latter of which contributes to Th1 polarization.Key words: CCR5 . CCR7 . NK-DC interaction . Th1 polarization Supporting Information available online Introduction NK cells are important effector cells in the innate immune response against virally infected or malignantly transformed cells and their cytotoxicity is regulated by a delicate balance of inhibitory and activating signals [1]. Recent studies suggest that the interplay between NK cells and DC, the specialized antigenpresenting cell of the innate immune system [2], is critical in shaping the adaptive immune response [3]. This concept originates from several lines of evidence including: the discovery of NK cells colocalizing with DC in the T-cell areas of lymph nodes [4,5], the coupling of NK-cell recruitment to lymph nodes Ã These authors contributed equally to this work. 3138with the induction of more potent Th1 skewing [3], and the identification of NK-cell subpopulations with helper properties [6]. Although the exact mechanisms of NK-DC interaction remain to be elucidated, increasing evidence supports the importance of bidirectional NK-DC crosstalk [7,8].On the one hand, NK-DC crosstalk is characterized by the capacity of activated NK cells to induce DC maturation with elevated IL-12p70 production and subsequently an increased capacity to induce Th1 and CTL responses [9]. This NK-induced DC maturation depends at least in part on soluble factors such as and as well as on engagement of the natural cytotoxicity triggering receptor 30 [12]. Moreover, NK cells control the quality of the adaptive immune response by natural cytotoxicity triggering receptor 30-mediated lysis of immature or inadequately matured DC [13], enabling only fully mature DC to migrate into lymph nodes and subsequently prime T cells. On the other hand, DC are able to induce NK-cell proliferation, augmentation of cytotoxicity and cytokine secretion [8]. The DC-induced modulati...

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Section: Discussionmentioning

confidence: 99%

“…In steady-state conditions, the CD56 bright CD16 À NK-cell subpopulation has been reported to express CCR7 [25], which allows them to migrate into lymph nodes [26]. However, in response to IL-18-producing monocytes, induction of CCR7 has also been observed on CD56 dim CD16 1 NK cells [6].…”

Section: Dc-dependent Induction Of Ccr7 Expression On Nk Cellsmentioning

confidence: 99%

Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells

et al. 2010

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“…17 After development, NK cells distribute widely throughout lymphoid and non-lymphoid tissues, including BM, lymph nodes (LN), spleen, peripheral blood, lung and liver. 18 NK cells, defined as CD3 2 CD56 1 lymphocytes, are distinguished as CD56 bright and CD56 dim subsets. Approximately 90% of peripheral blood and spleen NK cells belong to the CD56 dim CD16 1 subset with marked cytotoxic function upon interacting with target cells.…”

Section: Conception Of Nk Cellsmentioning

confidence: 99%

NK cell-based immunotherapy for malignant diseases

et al. 2013

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Natural killer (NK) cells play critical roles in host immunity against cancer. In response, cancers develop mechanisms to escape NK cell attack or induce defective NK cells. Current NK cell-based cancer immunotherapy aims to overcome NK cell paralysis using several approaches. One approach uses expanded allogeneic NK cells, which are not inhibited by self histocompatibility antigens like autologous NK cells, for adoptive cellular immunotherapy. Another adoptive transfer approach uses stable allogeneic NK cell lines, which is more practical for quality control and large-scale production. A third approach is genetic modification of fresh NK cells or NK cell lines to highly express cytokines, Fc receptors and/or chimeric tumor-antigen receptors. Therapeutic NK cells can be derived from various sources, including peripheral or cord blood cells, stem cells or even induced pluripotent stem cells (iPSCs), and a variety of stimulators can be used for large-scale production in laboratories or good manufacturing practice (GMP) facilities, including soluble growth factors, immobilized molecules or antibodies, and other cellular activators. A list of NK cell therapies to treat several types of cancer in clinical trials is reviewed here. Several different approaches to NK-based immunotherapy, such as tissue-specific NK cells, killer receptor-oriented NK cells and chemically treated NK cells, are discussed. A few new techniques or strategies to monitor NK cell therapy by non-invasive imaging, predetermine the efficiency of NK cell therapy by in vivo experiments and evaluate NK cell therapy approaches in clinical trials are also introduced.

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“…To determine if NK cells can also play a role in spread of T. gondii to the brain, we compared parasite loads in the brains of mice infected with free tachyzoites or with in vitro parasitized NK cells. Splenic NK cells were selected as, upon adoptive transfer, they have been shown to recirculate through all organs ordinarily containing NK cells 31. Previous studies showed that tachyzoites are detected in lymphoid tissues early after infection (between 2 and 6 days),4, 12, 32, 33 while parasites were detected in the brains of infected animals by 7 dpi 4, 8, 30, 34.…”

Section: Resultsmentioning

confidence: 99%

Parasitized Natural Killer cells do not facilitate the spread of Toxoplasma gondii to the brain

Petit-Jentreau

Glover

Coombes

2018

Parasite Immunology

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Summary Toxoplasma gondii is a protozoan parasite capable of invading immune cells and co‐opting their migratory pathways to disseminate through the host. Natural Killer (NK) cells can be directly invaded by the parasite and this invasion alters NK cell migration, producing a hypermotile phenotype. However, the consequences of this hypermotile phenotype for the dissemination of T. gondii to the brain remain unknown. To address this, C57BL6/J mice were infected with freshly egressed tachyzoites (type II Prugniaud strain) or with parasitized NK cells. Under both conditions, parasite loads in the brain were comparable, indicating that parasitized NK cells were not able to facilitate spread of T. gondii to the brain. Consistent with this, we found no evidence for the recruitment of endogenous NK cells to the brain at early time points post‐infection, nor any changes in the expression of α4β1 integrin, involved in recruitment of NK cells to the brain. We therefore found no evidence for a role for hypermotile NK cells in delivery of parasites to the brain during acute infection with T. gondii.

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The trafficking of natural killer cells

Cited by 472 publications

References 115 publications

Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells

Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells

NK cell-based immunotherapy for malignant diseases

Parasitized Natural Killer cells do not facilitate the spread of Toxoplasma gondii to the brain

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