• Corpus ID: 14537110

Lysis of tumor cells by natural killer cells in mice is impeded by platelets.

@article{Nieswandt1999LysisOT,
  title={Lysis of tumor cells by natural killer cells in mice is impeded by platelets.},
  author={Bernhard Nieswandt and Michael Hafner and Bernd Echtenacher and Daniela N M{\"a}nnel},
  journal={Cancer research},
  year={1999},
  volume={59 6},
  pages={
          1295-300
        }
}
Natural killer (NK) cells provide effective antitumoral activity in the blood stream of mice, leading to reduced metastasis. There are, however, tumor cells that metastasize despite the presence of an intact NK system. The capability of tumor cells to induce platelet aggregation, on the other hand, correlates with their enhanced metastatic potential. A counteractive role of platelets for the NK function in metastasis has never been conceived. Here we demonstrate for the first time that… 

Figures and Tables from this paper

Modulation of Natural Killer Cell Anti-Tumor Reactivity by Platelets
TLDR
The available data regarding tumor-platelet-NK cell interaction focusing on metastatic tumor spread is reviewed and the molecular mechanisms underlying this trilateral crosstalk are discussed.
Platelets and fibrin(ogen) increase metastatic potential by impeding natural killer cell-mediated elimination of tumor cells.
TLDR
These studies establish an important link between hemostatic factors and innate immunity and indicate that one mechanism by which the platelet-fibrin(ogen) axis contributes to metastatic potential is by impeding natural killer cell elimination of tumor cells.
Platelets and P-selectin control tumor cell metastasis in an organ-specific manner and independently of NK cells.
TLDR
It was found that platelets promote lung metastasis in the absence of NK cells in both acute and spontaneous metastasis models and it was shown that endothelial-derived P-selectin is just as important as platelet- derived P- selectin in promoting lung metastases and also plays an important role in liver metastasis.
Cells Inhibits NK Cell Antitumor Activity GITR Ligand Provided by Thrombopoietic
TLDR
This study shows that megakaryocytes acquire expression of the TNF family member gluco-corticoid-induced TNF-related ligand (GITRL) during differentiation, resulting in GITRL expression by platelets, and elucidates a novel mechanism by which host platelets may influence tumor–NK cell interaction and may facilitate tumor immune evasion.
Platelet-Mediated Protection of Cancer Cells From Immune Surveillance – Possible Implications for Cancer Immunotherapy
TLDR
The known interactions between platelets and NK cells in the solid tumor setting are reviewed and discussed and how these could also apply to hematological cancers.
NK Cell Interaction With Platelets and Myeloid Cells in the Tumor Milieu
TLDR
The underlying mechanisms of NK cell control by platelets and myeloid cells with focus on NKG2D and its ligands are discussed, and a timely perspective on how to harness these pathways with novel immunotherapeutic approaches is provided.
Platelet-derived transforming growth factor-beta down-regulates NKG2D thereby inhibiting natural killer cell antitumor reactivity.
TLDR
It is shown that platelet-derived soluble factors, secreted on coating of tumor cells or after stimulation with classic platelet agonists, impair NK cell antitumor reactivity resulting in diminished granule mobilization, cytotoxicity, and IFN-gamma production, and therapeutic intervention in tumor cell-platelet interaction and the resulting TGF-beta release by platelets may serve to enhance antitumors immunity.
Platelet-induced inhibition of tumor cell growth.
GITR Ligand Provided by Thrombopoietic Cells Inhibits NK Cell Antitumor Activity
TLDR
It is shown that megakaryocytes acquire expression of the TNF family member glucocorticoid-induced TNF-related ligand (GITRL) during differentiation, resulting in GITRL expression by platelets, which is identified as a mechanism by which platelets may alter tumor cell immunogenicity.
Inhibition of metastasis in a murine 4T1 breast cancer model by liposomes preventing tumor cell-platelet interactions
TLDR
It is concluded that Cil-L reduced metastasis by restricting the aggregability of mouse platelets, which probably prevents the interaction between circulating 4T1 tumor cells and Platelets, making the Cil -L a useful tool for the inhibition of breast cancer metastasis in mice.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 28 REFERENCES
Role of NK cells in tumour growth and metastasis in beige mice
TLDR
It is reported here that a tumour line, modified to be sensitive to NK cytotoxicity by in vitro culture, demonstrated in vivo an increased growth rate, faster induction time and an increased metastatic capability in bg compared to control mice.
TNF promotes metastasis by impairing natural killer cell activity
TLDR
Even though the metastasis‐enhancing effect of TNF remained detectable in mice which have a greatly reduced NK cell cytotoxic activity due to a defect in the bg locus, normal mice which were depleted of NK cells by antibody treatment did not show enhanced metastasis after TNF injection.
Regulation of natural killer function by nonlymphoid cells.
TLDR
Regulation of NK cells by nonlymphoid cells and their products likely provides an in vivo mechanism for locally regulating NK function.
Role of organ-associated NK cells in decreased formation of experimental metastases in lung and liver.
TLDR
The data are consistent with a role for organ-associated NK cells in inhibiting metastasis formation during the extravasation and/or early postextravasation phases of the metastatic process and suggest that organ- associated NK activity should be considered as a possible mechanism for the therapeutic effects of BRM treatment.
Role of adhesion molecules and platelets in TNF-induced adhesion of tumor cells to endothelial cells: implications for experimental metastasis.
TLDR
The correlation between inhibition of integrin binding and inhibition of metastasis achieved with competing peptides indicated an important role for extracellular matrix components in tumor cell attachment.
Target structures involved in natural killing (NK): characteristics, distribution, and candidate molecules.
TLDR
The proposed multifactorial nature of the NK cell-target cell interaction may represent the major complexity in the search for specific TS in natural killer cells.
Role of nk cells in the antimetastatic effect of anticoagulant drugs
TLDR
The antimetastatic effects of heparin and PGI2 are dependent on levels of NK activity in the host, and platelet aggregation and fibrin coating of the surface of tumor cells may be among the mechanisms by which hematogenously spread tumor cells are protected from destruction by NK cells.
Protection from tumor necrosis factor-mediated cytolysis by platelets.
TLDR
The role of associated platelets has to be considered when analyzing the cytotoxic and cytolytic activity of macrophage-derived TNF-alpha on tumor cells.
Functional role of platelets in experimental metastasis studied with cloned murine fibrosarcoma cell variants.
TLDR
It is suggested that platelets are required for successful lung colonization by highly metastatic clone PAK 17.15 cells, and this fibrosarcoma of high platelet aggregating-poorly metastatic cells, demonstrates that while the ability to aggregate platelets is necessary for successful metastasis by some tumor cells, it is insufficient if tumor cells lack other critical properties required for completion of the metastatic cascade.
Selective long-term elimination of natural killer cells in vivo by an anti-interleukin 2 receptor beta chain monoclonal antibody in mice
TLDR
It is found that NK and/or NK precursor cells become susceptible to the mAb treatment only after birth, suggesting that functional maturation of NK cells in terms of IL-2R beta expression is a later event in the course of NK cell development.
...
1
2
3
...