ArticleCancer immunology, immunotherapy : CII2010
FTY720 and SEW2871 reverse the inhibitory effect of S1P on natural killer cell mediated lysis of K562 tumor cells and dendritic cells but not on cytokine release.
Article in Cancer immunology, immunotherapy : CII, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
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- Drugs for Multiple Sclerosis Activate Natural Killer Cells: Do They Protect Against COVID-19 Infection?Infection and drug resistance · 2020Review
- S1PR1 as a Novel Promising Therapeutic Target in Cancer Therapy.Molecular diagnosis & therapy · 2019Review
- HCT-116 colorectal cancer cells secrete chemokines which induce chemoattraction and intracellular calcium mobilization in NK92 cells.Cancer immunology, immunotherapy : CII · 2019Article
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- Sphingosine-1 Phosphate: A New Modulator of Immune Plasticity in the Tumor Microenvironment.Frontiers in oncology · 2016Review
- Monomethyl fumarate augments NK cell lysis of tumor cells through degranulation and the upregulation of NKp46 and CD107a.Cellular & molecular immunology · 2016Article
- Suppression of natural killer cell cytotoxicity in postpartum women: time course and potential mechanisms.Biological research for nursing · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aims of this study are to examine the effect of sphingosine 1-phosphate (S1P) on IL-2-activated natural killer (NK) cell lysis of K562 tumor cells and immature dendritic cells (iDCs), and to investigate the mechanisms involved in S1P activity. Our results show that S1P protected K562 cells or iDCs from NK cell lysis, which was reversed by FTY720 and SEW2871, the antagonists of S1P(1). S1P did not modulate the expression of NKG2D, NKp30, NKp44 or CD158 on the surface of NK cells, and neither affected the expression of CD80, CD83, or CD86 on the surface of DCs. In contrast, it increased the expression of HLA-I and HLA-E on DCs, an activity that was inhibited by FTY720 or SEW2871. Similarly, the inhibitory effect of S1P for NK cell lysis of K562 cells was directed toward S1P(1) expressed on the tumor cells but not on NK cells. Further analysis indicates that NK cells secreted various cytokines and chemokines with various intensities: (1) low (IL-4, IL-6, IL-12, TNF-alpha and MCP-1); (2) intermediate (IL-1beta, IL-10, TGF-beta1, and IL-17A); (3) high (IFN-gamma, and MIP-1alpha); and (4) very high (MIP-1beta). S1P significantly reduced the release of IL-17A and IFN-gamma from NK cells, but this inhibition was S1P(1)-independent. These results indicate that S1P is an anti-inflammatory molecule, and that S1P(1) is important for the interaction among NK cells and tumor cells or DCs leading to up-regulation of HLA-I and HLA-E on the surface of DCs, but not in S1P inhibition of the release of inflammatory cytokines from NK cells. Further, the results suggest that FTY720 and SEW2871 may potentially be used as prophylactic and/or therapeutic drugs to treat cancer patients.
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