2019
DOI: 10.1002/jlb.mr0718-269r
|View full text |Cite
|
Sign up to set email alerts
|

Mechanisms of natural killer cell-mediated cellular cytotoxicity

Abstract: Cellular cytotoxicity, the ability to kill other cells, is an important effector mechanism of the immune system to combat viral infections and cancer. Cytotoxic T cells and natural killer (NK) cells are the major mediators of this activity. Here, we summarize the cytotoxic mechanisms of NK cells. NK cells can kill virally infected of transformed cells via the directed release of lytic granules or by inducing death receptor‐mediated apoptosis via the expression of Fas ligand or TRAIL. The biogenesis of perforin… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

7
317
1
1

Year Published

2019
2019
2024
2024

Publication Types

Select...
6
1

Relationship

0
7

Authors

Journals

citations
Cited by 354 publications
(325 citation statements)
references
References 166 publications
7
317
1
1
Order By: Relevance
“…NK cells have a wide array of inhibitory and stimulatory receptors on their cell surface that are used for immune surveillance. Upon activation, NK cells show potent cytolytic activity in response to infected or transformed cells by releasing cytotoxic perforin and granzyme and activating apoptotic pathways in target cells through the production of TNFα or via direct cell-cell contact through activation of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FASL) pathways [70,71]. Recent work has demonstrated important roles of PARP-1 in NK cell biology.…”
Section: Role Of Parp-1 and Parp-2 In The Cellular Components Of Thementioning
confidence: 99%
See 1 more Smart Citation
“…NK cells have a wide array of inhibitory and stimulatory receptors on their cell surface that are used for immune surveillance. Upon activation, NK cells show potent cytolytic activity in response to infected or transformed cells by releasing cytotoxic perforin and granzyme and activating apoptotic pathways in target cells through the production of TNFα or via direct cell-cell contact through activation of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FASL) pathways [70,71]. Recent work has demonstrated important roles of PARP-1 in NK cell biology.…”
Section: Role Of Parp-1 and Parp-2 In The Cellular Components Of Thementioning
confidence: 99%
“…Moreover, the PARP inhibitor Niraparib has been shown to enhance type I interferon signaling and T cell infiltration in the tumor and improve the therapeutic effect of anti-PD-1 [94]. NK cells can kill cancer cells by inducing death receptor-mediated apoptosis through the expression of FasL or TRAIL [71]. PARP inhibitors have been shown to sensitize cancer cells to death receptor-mediated apoptosis by upregulating death receptor surface expression [95,96] (Figure 4).…”
Section: Parp Inhibitors As Immunomodulatory Agentsmentioning
confidence: 99%
“…As we did not observe correlation between the expression of well-known NK cell-interacting surface ligands with the sensitivity of different target cell lines to distinct NK 8 cell cytotoxic modes, we next investigated the functional involvement of the key inhibitory and activating receptors on NK cell surface, as the target specificity could be conferred by surface ligands not in the profiling panel as discussed above. The NK cell receptors that we examined included two types of inhibitory receptors, KIRs and NKG2A (CD94), and three activating receptors important for cancer target recognition, including NKG2D (CD314), DNAM-1 (CD226) and NKp46 (CD335) [11,21]. Specifically, we used neutralizing antibodies to block individual receptors or combination of the receptors and then compared the extent and kinetics of target cell death via the three cytotoxic modes with those under the control condition (i.e., no receptor blocking).…”
Section: Target Dependence Of Nk Cell Cytotoxicity On Inhibitory Andmentioning
confidence: 99%
“…The Rac inhibitor, NSC23766, was from SelleckChem and used at 120 M for MCF7 and 50 M for SMMC-7721. Cells were pre-treated with either Y27632 for 1 hour or NSC23766 for [5][6][7][8][9][10][11][12] hours before experiments. The inhibitor of vacuolar type ATPase (V-ATPase), Concanamycin A, was from Santa Cruz Biotechnology.…”
Section: Chemicals and Neutralizing Antibodiesmentioning
confidence: 99%
See 1 more Smart Citation