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Mesenchymal stem cell-natural killer cell interactions: evidence that activated NK cells are capable of killing MSCs, whereas MSCs can inhibit IL-2-induced NK-cell proliferation.

It is shown that MSCs sharply inhibit IL-2-induced proliferation of resting NK cells, whereas they only partially affect the proliferation of activated NK cells.
PubMed (opens in a new tab)

Mesenchymal stem cells inhibit natural killer-cell proliferation, cytotoxicity, and cytokine production: role of indoleamine 2,3-dioxygenase and prostaglandin E2.

It is demonstrated that indoleamine 2,3-dioxygenase and prostaglandin E2 represent key mediators of the MSC-induced inhibition of NK cells, which prevents the induction of effector functions, such as cytotoxic activity and cytokine production.
PubMed (opens in a new tab)

MSCs inhibit monocyte-derived DC maturation and function by selectively interfering with the generation of immature DCs: central role of MSC-derived prostaglandin E2.

The role of MSCs in inhibiting early DC maturation is emphasized and the molecular mechanisms responsible for the inhibitory effect are identified, including PGE(2) and not IL-6 represents the key inhibitory mediator.
PubMed (opens in a new tab)

NCR+ILC3 concentrate in human lung cancer and associate with intratumoral lymphoid structures

It is shown that NCR+type 3 innate lymphoid cells display lymphoid tissue-inducing ability and are increased in early-stage human lung cancer, respond to cancer cells and associated fibroblasts by producing cytokines and are associated to intratumoural ectopic lymphoid structures.
Springer (opens in a new tab)

Expression of the DNAM-1 ligands, Nectin-2 (CD112) and poliovirus receptor (CD155), on dendritic cells: relevance for natural killer-dendritic cell interaction.

In cytolytic assays, DNAM-1 cooperated with NKp30 in the NK-mediated killing of both immature and mature DCs and the degree of contribution of DN AM-1 appeared to correlate with the surface densities of its specific ligands PVR and Nectin-2.
PubMed (opens in a new tab)

NK cell‐mediated lysis of autologous antigen‐presenting cells is triggered by the engagement of the phosphatidylinositol 3‐kinase upon ligation of the natural cytotoxicity receptors NKp30 and NKp46

Findings strongly suggest that NCR are responsible for the killing of autologous APC through the activation of PI‐3 K.
Wiley (opens in a new tab)

Mesenchymal Stromal Cells Induce Peculiar Alternatively Activated Macrophages Capable of Dampening Both Innate and Adaptive Immune Responses

The data show that MMSC induce the generation of a novel type of alternatively activated macrophages capable of suppressing both innate and adaptive immune responses, which may help to better understand the role of MSCs in healthy tissues and inflammatory diseases including cancer.
Wiley (opens in a new tab)

Analysis of the receptor-ligand interactions in the natural killer-mediated lysis of freshly isolated myeloid or lymphoblastic leukemias: evidence for the involvement of the Poliovirus receptor…

The size of the NK cell subset expressing the killer immunoglobulin-like receptor (KIR) not engaged by the HLA-class I alleles of the patient parallels the degree of NK cytotoxicity against leukemic cells.
PubMed (opens in a new tab)

IFN‐γ production in human NK cells through the engagement of CD8 by soluble or surface HLA class I molecules

Findings indicate that CD8 engagement by sHLA‐I activates a cyclosporin A‐dependent pathway leading to production and secretion of IFN‐γ which may play a role in the regulation of innate immune responses in humans.
Wiley (opens in a new tab)

Mesenchymal stem cells inhibit natural killer – cell proliferation , cytotoxicity , and cytokine production : role of indoleamine 2 , 3-dioxygenase and prostaglandin E 2

It is shown that MSCs not only inhibit the cytokine-induced proliferation of freshly isolated NK cells but also prevent the induction of effector functions, such as cytotoxic activity and cytokine production, which are related to a sharp downregulation of the surface expression of the activating NK receptors NKp30, NKp44, and NKG2D.
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