Regulation of FasL expression in natural killer cells

Chua, Hui Lin; Serov, Youri A.; Brahmi, Zacharie

doi:10.1016/j.humimm.2004.01.004

Cited by 31 publications

(24 citation statements)

References 54 publications

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“…FasL, in particular, is expressed both by osteoclasts [31], which participate in bone remodeling, and by activated lymphocytes [70,71], which are recruited during inflammation. FasL is also expressed by CD34ϩ bone marrow cells [72] and thus may be present when marrow is included in bone grafts [11,39].…”

Section: Discussionmentioning

confidence: 99%

Tethered Epidermal Growth Factor Provides a Survival Advantage to Mesenchymal Stem Cells

et al. 2007

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MSC can act as a pluripotent source of reparative cells during injury and therefore have great potential in regenerative medicine and tissue engineering. However, the response of MSC to many growth factors and cytokines is unknown. Many envisioned applications of MSC, such as treating large defects in bone, involve in vivo implantation of MSC attached to a scaffold, a process that creates an acute inflammatory environment that may be hostile to MSC survival. Here, we investigated cellular responses of MSC on a biomaterial surface covalently modified with epidermal growth factor (EGF). We found that surfacetethered EGF promotes both cell spreading and survival more strongly than saturating concentrations of soluble EGF. By sustaining mitogen-activated protein kinase kinase-extracellular-regulated kinase signaling, tethered EGF increases the contact of MSC with an otherwise moderately adhesive synthetic polymer and confers resistance to cell death induced by the proinflammatory cytokine, Fas ligand. We concluded that tethered EGF may offer a protective advantage to MSC in vivo during acute inflammatory reactions to tissue engineering scaffolds. The tethered EGF-modified polymers described here could be used together with structural materials to construct MSC scaffolds for the treatment of hard-tissue lesions, such as large bony defects.

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Section: Discussionmentioning

confidence: 99%

Tethered Epidermal Growth Factor Provides a Survival Advantage to Mesenchymal Stem Cells

et al. 2007

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“…Expression of FasL was observed to be upregulated upon NK cell activation by stimulating the cells with PMA/ionomycin, with cytokines, or by cross-linking different activating receptors (see, e.g. [37], [38]). Thus, FasL expression may be regulated by the presence of target cells.…”

Section: Discussionmentioning

confidence: 99%

Human NK Cells Differ More in Their KIR2DL1-Dependent Thresholds for HLA-Cw6-Mediated Inhibition than in Their Maximal Killing Capacity

et al. 2011

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In this study we have addressed the question of how activation and inhibition of human NK cells is regulated by the expression level of MHC class I protein on target cells. Using target cell transfectants sorted to stably express different levels of the MHC class I protein HLA-Cw6, we show that induction of degranulation and that of IFN-γ secretion are not correlated. In contrast, the inhibition of these two processes by MHC class-I occurs at the same level of class I MHC protein. Primary human NK cell clones were found to differ in the amount of target MHC class I protein required for their inhibition, rather than in their maximum killing capacity. Importantly, we show that KIR2DL1 expression determines the thresholds (in terms of MHC I protein levels) required for NK cell inhibition, while the expression of other receptors such as LIR1 is less important. Furthermore, using mathematical models to explore the dynamics of target cell killing, we found that the observed delay in target cell killing is exhibited by a model in which NK cells require some activation or priming, such that each cell can lyse a target cell only after being activated by a first encounter with the same or a different target cell, but not by models which lack this feature.

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“…Natural killer cells can bind target cells through β 1 and β 2 integrins, including α 4 β 1 RGD-independent), which are selective toward multiple intercellular adhesion molecules (Genego, 2010) and are important for proper adhesion of NK cells to target cells (Chong et al, 1994; Gismondi et al, 2003; Somersalo et al, 1995). In addition to adhesion, activation of α 4 β 1 signaling may also cause the transcription of cytokines, such as interleukin-8, via the mitogen-activated protein kinase pathway, which plays a role in NK cytotoxicity (Mainiero et al, 1998, 2000; Chua et al, 2004). Interestingly, α 4 β 1 was proposed by Danen et al (1998) as a possible target for eristostatin binding to MV3 melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of the disintegrin eristostatin on melanoma–natural killer cell interactions

Hailey

Adams

Penn

et al. 2013

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Malignant melanoma is difficult to treat due to its resistance to chemotherapeutic regimens. Discovery of new pharmaceuticals with inhibitory potential can be helpful in the development of novel treatments. The snake venom disintegrin eristostatin, from the viper Eristicophis macmahoni, caused immunodeficient mice to be significantly protected from development of lung colonization when melanoma cells and the disintegrin were coinjected in vivo into the lateral tail vein compared to vehicle controls. Cytotoxicity assays suggested that eristostatin makes the melanoma cells a better target for lysis by human natural killer cells. Direct binding assays using atomic force microscopy showed eristostatin does specifically bind the surface of the six melanoma cell lines tested. Eristostatin binding was partially inhibited by the addition of soluble RGDS peptide, suggesting an integrin as one likely, but not the sole, binding partner. Studies done with melanoma cells on a culture dish and natural killer cells attached to a cantilever tip in atomic force microscopy showed four major populations of interactions which exhibited altered frequency and unbinding strength in the presence of eristostatin.

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Regulation of FasL expression in natural killer cells

Cited by 31 publications

References 54 publications

Tethered Epidermal Growth Factor Provides a Survival Advantage to Mesenchymal Stem Cells

Tethered Epidermal Growth Factor Provides a Survival Advantage to Mesenchymal Stem Cells

Human NK Cells Differ More in Their KIR2DL1-Dependent Thresholds for HLA-Cw6-Mediated Inhibition than in Their Maximal Killing Capacity

Effect of the disintegrin eristostatin on melanoma–natural killer cell interactions

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