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 (CD155) and Nectin-2 (CD112)

Pende, Daniela; Spaggiari, Grazia Maria; Marcenaro, Stefania; Martini, Stefania; Rivera, Paola; Capobianco, Andrea; Falco, Michela; Lanino, Edoardo; Pierri, Ivana; Zambello, Renato; Bacigalupo, Andrea; Mingari, Maria Cristina; Moretta, Alessandro; Moretta, Lorenzo

doi:10.1182/blood-2004-09-3548

Cited by 338 publications

(368 citation statements)

References 39 publications

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“…27 Together with the activating NK cell receptor NKG2D, these are the main receptors involved in NK cell-mediated recognition and killing of leukemic target cells. 28 Importantly, NCR downregulation (NCR dull ) on NK cells was found to be associated with poor prognosis for AML patients, as NCR dull AML patients showed significantly lower 5-year survival rates than their NCR bright counterparts. 25 Besides the activating receptor status, the inhibitory receptor phenotype also has a role in the escape of AML from NK cells.…”

Section: How Aml Evades Nk Cell Immune Surveillancementioning

confidence: 99%

“…40,41 AML cells themselves contribute to impaired NK cell-mediated killing by decreased or absent expression of surface ligands for various NK cell activating receptors, including NCRs and NKG2D. 27,28,42,43 Furthermore, AML cells can shed ligands for NKG2D, as demonstrated by the increased serum levels of MHC class I chain-related genes A and B (MICA/B) in AML patients compared with healthy controls. 43,44 These soluble ligands may provide a chronic systemic stimulus to NK cells resulting in reduced receptor expression and impaired NK cell-mediated cytotoxicity (Table 1).…”

Section: How Aml Evades Nk Cell Immune Surveillancementioning

confidence: 99%

“…97 In analogy with the lowered activating receptor expression, surface expression of NKG2D ligands (MIC and ULBP molecules) is low or absent on AML blasts and is related to impaired NK cell-mediated cytotoxicity (Table 1). 28,[42][43][44]98 In addition, secretion of soluble NKG2D ligands in AML contributes to evasion of NK cell surveillance (Table 1). 43,44 In this regard, an attractive immunotherapy would be to upregulate these ligands on AML cells to enhance their susceptibility to NK cell recognition and restore their sensitivity to NK cell killing.…”

Section: Nk Cell Immune Escape In Aml E Lion Et Almentioning

confidence: 99%

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Natural killer cell immune escape in acute myeloid leukemia

et al. 2012

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Section: How Aml Evades Nk Cell Immune Surveillancementioning

confidence: 99%

Section: How Aml Evades Nk Cell Immune Surveillancementioning

confidence: 99%

Section: Nk Cell Immune Escape In Aml E Lion Et Almentioning

confidence: 99%

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Natural killer cell immune escape in acute myeloid leukemia

et al. 2012

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“…The presence of alloreactive NK cells can be predicted by the analysis of the donor KIR gene profile and by the HLA class I typing of both donor and recipient. The actual presence and size of the alloreactive NK subset can be assessed by cytofluorimetric analysis using appropriate combinations of anti-KIR mAb (14,(36)(37)(38)(39)(40). In these experiments, alloreactive NK cells are identified as a subset expressing iKIRs specific for the mismatched KIR ligand but missing all the other iKIRs and NKG2A.…”

mentioning

confidence: 99%

Combined Genotypic and Phenotypic Killer Cell Ig-Like Receptor Analyses Reveal KIR2DL3 Alleles Displaying Unexpected Monoclonal Antibody Reactivity: Identification of the Amino Acid Residues Critical for Staining

Falco

Romeo

Marcenaro³

et al. 2010

The Journal of Immunology

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In humans, recent clinical and experimental data from hematopoietic stem cell transplantation revealed that donor-derived alloreactive NK cells exert a beneficial graft versus leukemia effect. The existence of donor-derived alloreactive NK cells can be predicted on the basis of donor killer cell Ig-like receptor (KIR) gene profile and HLA class I typing of both donor and recipient. Moreover, the size of the alloreactive NK cell population can be directly assessed by the combined use of anti–KIR-specific mAb. In this study, in an attempt to improve the definition of alloreactive NK cell subsets, we assessed the KIR genotype and phenotype in a cohort of 44 donors. This approach allowed the identification of two different KIR2DL3 alleles (KIR2DL3*005 and the novel allele KIR2DL3*015) that did not react with the anti–KIR2DL3-specific ECM41 mAb. In contrast, both alleles were recognized at the cell surface by several mAb reacting with KIR2DL2/L3/S2. Notably, KIR2DL3*005 was also stained by the anti–KIR2DL1/S1-specific EB6B and 11PB6 mAb. Functional analysis revealed that, despite its particular mAb reactivity, the specificity of KIR2DL3*005 for HLA-C molecules did not differ from that of other KIR2DL2/L3 alleles. Finally, site-directed mutagenesis demonstrated that glutamine at position 35 is required for ECM41 staining, whereas glutamic acid 35 and arginine 50 are relevant for staining with EB6B or 11PB6 mAb. Our present data represent a substantial progress in the characterization of the NK cell repertoire and an improved phenotypic/functional definition of given KIR+ subsets.

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“…This property has recently received a great deal of attention. [42][43][44] In vivo experiments using syngeneic mice also indicated that CD112-or CD155-transduced RMA tumor cells could be rejected by CD226-expressing CD8 1 T and NK cells. 45 It should be noted that CD226 could not induce cytotoxicity by resting NK cells.…”

Section: Interaction Of Cd226 and Cd96 With Their Ligand Mediates Mulmentioning

confidence: 99%

A novel interface consisting of homologous immunoglobulin superfamily members with multiple functions

Jin

2010

Cell Mol Immunol

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Immunoglobulin superfamily (IgSF) members account for a large proportion of cell adhesion molecules that perform important immunological functions, including recognizing a variety of counterpart molecules on the cell surface or extracellular matrix. The findings that CD155/poliovirus receptor (PVR) and CD112/nectin-2 are the ligands for CD226/platelet and T-cell activation antigen 1 (PTA1)/DNAX accessory molecular-1 (DNAM-1), CD96/tactile and Washington University cell adhesion molecule (WUCAM) and that CD226 is physically and functionally associated with lymphocyte function-associated antigen-1 (LFA-1) on natural killer (NK) and activated T cells have largely expanded our knowledge about the functions of CD226, CD96, WUCAM and LFA-1 and their respective ligands, CD155, CD112, intercellular adhesion molecule (ICAM)-1 and junctional adhesion molecule (JAM)-1. The interactions of these receptors and their ligands are involved in many key functions of immune cells including naive T

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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 (CD155) and Nectin-2 (CD112)

Cited by 338 publications

References 39 publications

Natural killer cell immune escape in acute myeloid leukemia

Natural killer cell immune escape in acute myeloid leukemia

Combined Genotypic and Phenotypic Killer Cell Ig-Like Receptor Analyses Reveal KIR2DL3 Alleles Displaying Unexpected Monoclonal Antibody Reactivity: Identification of the Amino Acid Residues Critical for Staining

A novel interface consisting of homologous immunoglobulin superfamily members with multiple functions

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