Identification of a cellular ligand for the natural cytotoxicity receptor NKp44

Baychelier, Florence; Sennepin, Alexis; Ermonval, Myriam; Dorgham, Karim; Debré, Patrice; Vieillard, Vincent

doi:10.1182/blood-2013-03-489054

Cited by 147 publications

(137 citation statements)

References 47 publications

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“…3G). Differently from K562 target cells, HEK 293T cell line expresses ligands for both NKp44 and NKG2D (38,49,50). Therefore, the degree of CD107a pos M1-primed NK cells was significantly reduced in the presence of NKp44 masking and was restored to almost basal levels when NKp44 and NKG2D were blocked together (Fig.…”

Section: M1 Macrophages Induce Nkp44 and Nkg2d Upregulation Via Il-1bmentioning

confidence: 87%

Priming of Human Resting NK Cells by Autologous M1 Macrophages via the Engagement of IL-1β, IFN-β, and IL-15 Pathways

Mattiola

Pesant

Tentorio

et al. 2015

The Journal of Immunology

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The cross talk between NK cells and macrophages is emerging as a major line of defense against microbial infections and tumors. This study reveals a complex network of soluble mediators and cell-to-cell interactions allowing human classically activated (M1) macrophages, but not resting (M0) or alternatively activated (M2) macrophages, to prime resting autologous NK cells. In this article, we show that M1 increase NK cell cytotoxicity by IL-23 and IFN-β-dependent upregulation of NKG2D, IL-1β-dependent upregulation of NKp44, and trans-presentation of IL-15. Moreover, both IFN-β-dependent cis-presentation of IL-15 on NK cells and engagement of the 2B4-CD48 pathway are used by M1 to trigger NK cell production of IFN-γ. The disclosure of these synergic cellular mechanisms regulating the M1-NK cell cross talk provides novel insights to better understand the role of innate immune responses in the physiopathology of tumor biology and microbial infections

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Section: M1 Macrophages Induce Nkp44 and Nkg2d Upregulation Via Il-1bmentioning

confidence: 87%

Priming of Human Resting NK Cells by Autologous M1 Macrophages via the Engagement of IL-1β, IFN-β, and IL-15 Pathways

Mattiola

Pesant

Tentorio

et al. 2015

The Journal of Immunology

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“…23 On the other hand, molecularly unrelated cellular ligands have been shown to bind NKp30 (B7H6 and BAT3/BAG6) and NKp44 (21spe-MLL5). 24-26 …”

Section: Introductionmentioning

confidence: 99%

Nidogen-1 is a novel extracellular ligand for the NKp44 activating receptor

et al. 2018

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The release of soluble ligands of activating Natural Killer (NK) cell receptors may represent a regulatory mechanism of NK cell function both in physiologic and in pathologic conditions. Here, we identified the extracellular matrix protein Nidogen-1 (NID1) as a ligand of NKp44, an important activating receptor expressed by activated NK cells. When released as soluble molecule, NID1 regulates NK cell function by modulating NKp44-induced IFN-γ production or cytotoxicity. In particular, it also modulates IFN-γ production induced by Platelet-Derived Growth Factor (PDGF)-DD following NKp44 engagement. We also show that NID1 may be present at the cell surface. In this form or when bound to a solid support (bNID1), NID1 fails to induce NK cell cytotoxicity or cytokine release. However, analysis by mass spectrometry revealed that exposure to bNID1 can induce in human NK cells relevant changes in the proteomic profiles suggesting an effect on different biological processes.

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“…Although NCRs were found to bind some viral glycoproteins, their ligands on tumour cells have only partially been defined 10,11 . B7-H6 and, very recently, a novel isoform of the mixed-lineage leukemia (MLL5) protein have been shown to be expressed on a large panel of tumour cells 12,13 and are recognized by NKp30 and NKp44 receptors, respectively. Although a role of NK cells in anti-tumour immunity has been established, such a role for other ILC populations remains largely unexplored.…”

mentioning

confidence: 99%

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

et al. 2015

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Tertiary lymphoid structures (TLSs) are a common finding in non-small cell lung cancer (NSCLC) and are predictors of favourable clinical outcome. Here we show that NCR þ innate lymphoid cell (ILC)-3 are present in the lymphoid infiltrate of human NSCLC and are mainly localized at the edge of tumour-associated TLSs. This intra-tumoral lymphocyte subset is endowed with lymphoid tissue-inducing properties and, on activation, produces IL-22, TNF-a, IL-8 and IL-2, and activates endothelial cells. Tumour NCR þ ILC3 may interact with both lung tumour cells and tumour-associated fibroblasts, resulting in the release of cytokines primarily on engagement of the NKp44-activating receptor. In patients, NCR þ ILC3 are present in significantly higher amounts in stage I/II NSCLC than in more advanced tumour stages and their presence correlate with the density of intratumoral TLSs. Our results indicate that NCR þ ILC3 accumulate in human NSCLC tissue and might contribute to the formation of protective tumour-associated TLSs.

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Identification of a cellular ligand for the natural cytotoxicity receptor NKp44

Cited by 147 publications

References 47 publications

Priming of Human Resting NK Cells by Autologous M1 Macrophages via the Engagement of IL-1β, IFN-β, and IL-15 Pathways

Priming of Human Resting NK Cells by Autologous M1 Macrophages via the Engagement of IL-1β, IFN-β, and IL-15 Pathways

Nidogen-1 is a novel extracellular ligand for the NKp44 activating receptor

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

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