Targeting RNA polymerase I to boost natural killer cell anticancer activity in multiple myeloma Elena Sproviero, Eleonora Gnocchini, Tommaso Cipollone, Sara Petillo, Chiara Cassone, Rosa Molfetta, Alessandra Zingoni, Alessandra Soriani, Cristina Cerboni, Maria Teresa Petrucci, Francesca Fazio, Rossella Paolini, Gabriella Palmieri, Marco Cippitelli Cell Death and Disease, 2025 Multiple myeloma (MM) remains an incurable disease despite therapeutic advancements extending survival. Relapses driven by drug resistance and minimal residual disease underscore the need for novel treatment strategies. Natural Killer (NK) cells play a key role in MM immunity, yet their function is suppressed by inhibitory cytokines and metabolites from the tumor microenvironment. Developing anticancer drugs with immunomodulatory properties, such as enhancing tumor sensitivity to NK cell recognition, remains a critical challenge. MM cells exhibit high protein synthesis rates, making them vulnerable to proteostasis disruption. Dysregulated ribosome function and aberrant mRNA translation contribute to proteasome inhibitor resistance. RNA Polymerase I (RNA Pol I)-mediated rDNA transcription, the rate-limiting step in ribosome biogenesis (RiBi), is significantly upregulated in MM. Targeting rDNA transcription and inducing nucleolar stress response (NSR) presents a promising therapeutic approach, though its immunomodulatory role is not well understood. Our study examined two “first-in-cla ss ” RNA Pol I inhibitors, CX-5461 and BMH-21, which differentially regulate NK cell-activating and inhibitory ligand expression in MM. BMH-21 enhanced NK cell degranulation and increased IFN-γ and TNF-α secretion, demonstrating stronger immunostimulatory effects than CX-5461. Conversely, CX-5461 induced a significant DNA damage response (DDR) and senescence, leading to HLA-E upregulation and suppressing NK cell activity. Mechanistic analyses revealed that HLA-E presentation is governed by ATR/AKT/mTORC1/S6K signaling and Pioneer Round of Translation (PRT), linking its regulation to DDR. This effect was modulated by Lenalidomide and Panobinostat. Moreover, RNA Pol I inhibition enhanced Daratumumab-mediated antibody-dependent cellular cytotoxicity (ADCC) of NK cells against MM, uncovering novel immuno-mediated antitumor mechanisms.
Precondensed Plasmid DNA Enhances CAR-T Cell Generation via Lipid Nanoparticles Andrea Pirrottina, Serena Renzi, Luca Digiacomo, Francesca Giulimondi, Valentina De Lorenzi, Samuele Ghignoli, Luca Pesce, Francesco Cardarelli, Francesco Mura, Giacomo Parisi, Luca Buccini, Chiara Cassone, Alessandra Zingoni, Daniela Pozzi, Giulio Caracciolo ACS Omega, 2025 The advent of chimeric antigen receptor (CAR) T-cell therapy has introduced a novel and personalized approach to cancer treatment. Despite its promise, the challenge of developing a system that bypasses the need for viral vectors remains significant, particularly in terms of achieving a clinical efficacy and sustained durability. To address these challenges, lipid nanoparticles (LNPs) produced through advanced microfluidic technology have been recently utilized to encapsulate plasmid DNA (pDNA) encoding CAR receptors. However, the intrinsic challenges associated with pDNA encapsulation, along with the critical requirement for efficient expression, remain substantial obstacles. Here, we show that incorporating DNA-condensing agents into the microfluidic manufacturing of LNPs effectively overcomes these limitations. Briefly, we conducted a preliminary investigation to characterize LNPs with and without the commercial condensing agent P3000-Reagent (PR), focusing on their physicochemical properties and scrutinizing the biological outcomes primarily in the HEK-293 cell line. Our results demonstrated that precondensation of the pDNA with PR differentially increased the transfection efficiency of the tested formulations, whereas confocal microscopy indicated reduced lysosomal colocalization and major nuclear localization. Finally, PR was found to enhance LNP efficiency upon multiple administrations to the immortalized T-lymphocyte Jurkat cell line, enabling the delivery of both a luciferase reporter gene and a functional CAR-encoding plasmid. Overall, these findings underscore the great potential of introducing DNA-condensing agents into the LNP preparation process, especially for systems designed for challenging delivery applications, such as multiadministration transfection protocols.
ADAR1 expression is associated with cervical cancer progression and negatively regulates NK cell activity Valentina Tassinari, Marta Kaciulis, Stefano Petrai, Helena Stabile, Angelina Pernazza, Martina Leopizzi, Valeria Di Maio, Francesca Belleudi, Danilo Ranieri, Vanessa Mancini, Innocenza Palaia, Federica Tanzi, Ludovica Lospinoso Severini, Silvia Ruggeri, Maria Emanuela Greco, Giovanni Bernardini, Alessandra Zingoni, Marco Cippitelli, Cristina Cerboni, Alessandra Soriani Jci Insight, 2025 ADAR1 edits double-stranded RNAs (dsRNAs) by deaminating adenosines into inosines, preventing aberrant activation of innate immunity by endogenous dsRNAs, which may resemble viral structures. Several tumors exploit ADAR1 to evade immune surveillance; indeed, its deletion reduces tumor viability and reshapes infiltrating leukocytes. Here we investigated the role of ADAR1 in immune evasion mechanisms during cervical cancer (CC) progression. Patients’ biopsy samples showed higher ADAR1 expression already in premalignant lesions (squamous intraepithelial lesions [SIL]) and a substantially reduced percentage of infiltrating CD7+ innate cells in in situ and invasive carcinomas compared with normal mucosa, with CD56+ NK cells showing phenotypic alterations that may have affected their functional responses. In CC-derived cell lines (SiHa, CaSki), ADAR1 silencing reduced cell proliferation, an effect further enhanced by exogenous IFN-β administration. It also induced proinflammatory gene expression, as demonstrated by RNA-Seq analysis, and conditioned supernatants collected from these cells activated several NK cell effector functions. NK cell infiltration and activation were also confirmed in organotypic 3D tissue models of SiHa cells knocked out for ADAR1. In conclusion, ADAR1 expression increased with CC progression and was accompanied by alterations in tumor-infiltrating NK cells, but its silencing in CC-derived cell lines potentiated antitumor NK cell activities. Thus, ADAR1 inhibition may represent a therapeutic perspective for CC and possibly other malignancies.
Protein-DNA Competition at the Bio-Nano Interface: Structural and Biological Insights From Graphene Oxide Coronas Erica Quagliarini, Francesca Giulimondi, Serena Renzi, Andrea Pirrottina, Alessandra Zingoni, Nicholas Carboni, Daniela Pozzi, Giulio Caracciolo Advanced Materials Interfaces, 2025 Understanding interactions between nanomaterials and biomolecules is essential for advancing biomedical nanotechnologies. This study investigates how double‐stranded DNA of varying sizes affects the protein corona (PC) surrounding Graphene Oxide (GO) nanosheets in DNA‐supplemented human plasma. The findings reveal that DNA plays a pivotal role in modulating the PC composition through dynamic competition governed by factors like surface charge, affinity, and DNA fragment size. At lower DNA concentrations, competition between DNA and proteins for binding sites on GO leads to a corona predominantly composed of proteins, with some DNA molecules also bound. However, as the DNA concentration increases beyond a threshold, a shift occurs. DNA increasingly outcompetes proteins for binding sites, resulting in a two‐component corona enriched with both DNA and proteins. Notably, the proportion of DNA within the corona progressively increases with rising DNA concentration, while the protein content decreases. This dynamic interplay between DNA and proteins has significant biological implications. A monotonic increase in Toll‐like receptor 9 (TLR9) activation is observed as the DNA content within the corona increases. As the corona composition and its influence on cellular responses are crucial, this study emphasizes the relevance of exploring competition at the bio‐nano interface for the advancement of these applications.
NKG2D triggering hampers DNAM-1-mediated signaling in human NK cells Caterina Marangio, Nadia Domenica Milito, Erisa Putro, Alessia Carnevale, Cristina Capuano, Alessandra Zingoni, Marco Cippitelli, Angela Santoni, Rossella Paolini, Rosa Molfetta Frontiers in Immunology, 2025 IntroductionNatural Killer (NK) cells are cytotoxic innate lymphocytes able to detect transformed cells through the balanced action of inhibitory and activating receptors. NKG2D is one of the main activating receptors involved in tumor surveillance thanks to its ability to recognize stress-induced ligands. Of note, the prolonged exposure to NKG2D ligands promotes receptor down-modulation that results in defective activation of NKG2D and other unrelated activating receptors, including DNAM-1 that is also involved in tumor clearance. However, further investigations are necessary to characterize how the NKG2D/DNAM-1 interplay affects NK cell anti-tumor function.MethodsPrimary cultured human NK cells were stimulated with the natural ligand MICA or an anti-NKG2D agonist antibody. The expression of activating and inhibitory receptors as well as DNAM-1-triggered signaling events and cytotoxicity were evaluated by flow cytometry. DNAM-1-mediated granule polarization was evaluated by confocal microscopy.ResultsWe showed that NKG2D crosslinking mediated by the natural ligand MICA or an agonist antibody had different consequences on primary cultured human NK cells. Indeed, MICA stimulation increases the expression of the checkpoint receptor TIGIT that is able to counteract DNAM-1 activation. Stimulation with the agonist antibody, without altering TIGIT expression, directly inhibits DNAM-1-mediated signal transduction and cytotoxic function with a mechanism that required NKG2D endocytosis.DiscussionOur findings contribute to shed light on the functional consequences of NKG2D engagement, demonstrating that a direct impact on DNAM-1-mediated signal transduction occurs independently from the modality of NKG2D crosslinking. Understanding the molecular mechanisms responsible for suppression of NK cell activation may help the development of therapeutic anti-cancer strategies aimed to prevent NK cell dysfunction or to reinvigorate an impaired cytotoxic activity.
The senescence journey in cancer immunoediting Alessandra Zingoni, Fabrizio Antonangeli, Silvano Sozzani, Angela Santoni, Marco Cippitelli, Alessandra Soriani Molecular Cancer, 2024 Cancer progression is continuously controlled by the immune system which can identify and destroy nascent tumor cells or inhibit metastatic spreading. However, the immune system and its deregulated activity in the tumor microenvironment can also promote tumor progression favoring the outgrowth of cancers capable of escaping immune control, in a process termed cancer immunoediting. This process, which has been classified into three phases, i.e. “elimination”, “equilibrium” and “escape”, is influenced by several cancer- and microenvironment-dependent factors. Senescence is a cellular program primed by cells in response to different pathophysiological stimuli, which is based on long-lasting cell cycle arrest and the secretion of numerous bioactive and inflammatory molecules. Because of this, cellular senescence is a potent immunomodulatory factor promptly recruiting immune cells and actively promoting tissue remodeling. In the context of cancer, these functions can lead to both cancer immunosurveillance and immunosuppression. In this review, the authors will discuss the role of senescence in cancer immunoediting, highlighting its context- and timing-dependent effects on the different three phases, describing how senescent cells promote immune cell recruitment for cancer cell elimination or sustain tumor microenvironment inflammation for immune escape. A potential contribution of senescent cells in cancer dormancy, as a mechanism of therapy resistance and cancer relapse, will be discussed with the final objective to unravel the immunotherapeutic implications of senescence modulation in cancer.
Structuring lipid nanoparticles, DNA, and protein corona into stealth bionanoarchitectures for in vivo gene delivery Serena Renzi, Luca Digiacomo, Daniela Pozzi, Erica Quagliarini, Elisabetta Vulpis, Maria Valeria Giuli, Angelica Mancusi, Bianca Natiello, Maria Gemma Pignataro, Gianluca Canettieri, Laura Di Magno, Luca Pesce, Valentina De Lorenzi, Samuele Ghignoli, Luisa Loconte, Carmela Maria Montone, Anna Laura Capriotti, Aldo Laganà, Carmine Nicoletti, Heinz Amenitsch, Marco Rossi, Francesco Mura, Giacomo Parisi, Francesco Cardarelli, Alessandra Zingoni, Saula Checquolo, Giulio Caracciolo Nature Communications, 2024 Lipid nanoparticles (LNPs) play a crucial role in addressing genetic disorders, and cancer, and combating pandemics such as COVID-19 and its variants. Yet, the ability of LNPs to effectively encapsulate large-size DNA molecules remains elusive. This is a significant limitation, as the successful delivery of large-size DNA holds immense potential for gene therapy. To address this gap, the present study focuses on the design of PEGylated LNPs, incorporating large-sized DNA, departing from traditional RNA and ionizable lipids. The resultant LNPs demonstrate a unique particle morphology. These particles were further engineered with a DNA coating and plasma proteins. This multicomponent bionanoconstruct exhibits enhanced transfection efficiency and safety in controlled laboratory settings and improved immune system evasion in in vivo tests. These findings provide valuable insights for the design and development of bionanoarchitectures for large-size DNA delivery, opening new avenues for transformative gene therapies. Encapsulation of large-size DNA molecules into lipid nanoparticles (LNPs) remains challenging. Here, the authors engineer PEGylated LNPs with DNA and plasma proteins to improve the delivery of large DNA molecules, enhancing the gene therapy potential.
Optimizing Transfection Efficiency in CAR-T Cell Manufacturing through Multiple Administrations of Lipid-Based Nanoparticles Francesca Giulimondi, Luca Digiacomo, Serena Renzi, Chiara Cassone, Andrea Pirrottina, Rosa Molfetta, Ilaria Elena Palamà, Gabriele Maiorano, Giuseppe Gigli, Heinz Amenitsch, Daniela Pozzi, Alessandra Zingoni, Giulio Caracciolo ACS Applied Bio Materials, 2024 The existing manufacturing protocols for CAR-T cell therapies pose notable challenges, particularly in attaining a transient transfection that endures for a significant duration. To address this gap, this study aims to formulate a transfection protocol utilizing multiple lipid-based nanoparticles (LNPs) administrations to enhance transfection efficiency (TE) to clinically relevant levels. By systematically fine-tuning and optimizing our transfection protocol through a series of iterative refinements, we have accomplished a remarkable one-order-of-magnitude augmentation in TE within the immortalized T-lymphocyte Jurkat cell line. This enhancement has been consistently observed over 2 weeks, and importantly, it has been achieved without any detrimental impact on cell viability. In the subsequent phase of our study, we aimed to optimize the gene delivery system by evaluating three lipid-based formulations tailored for DNA encapsulation using our refined protocol. These formulations encompassed two LNPs constructed from ionizable lipids and featuring systematic variations in lipid composition (iLNPs) and a cationic lipoplex (cLNP). Our findings showcased a notable standout among the three formulations, with cLNP emerging as a frontrunner for further refinement and integration into the production pipeline of CAR-T therapies. Consequently, cLNP was scrutinized for its potential to deliver CAR-encoding plasmid DNA to the HEK-293 cell line. Confocal microscopy experiments demonstrated its efficiency, revealing substantial internalization compared to iLNPs. By employing a recently developed confocal image analysis method, we substantiated that cellular entry of cLNP predominantly occurs through macropinocytosis. This mechanism leads to heightened intracellular endosomal escape and mitigates lysosomal accumulation. The successful expression of anti-CD19-CD28-CD3z, a CAR engineered to target CD19, a protein often expressed on the surface of B cells, was confirmed using a fluorescence-based assay. Overall, our results indicated the effectiveness of cLNP in gene delivery and suggested the potential of multiple administration transfection as a practical approach for refining T-cell engineering protocols in CAR therapies. Future investigations may focus on refining outcomes by adjusting transfection parameters like nucleic acid concentration, lipid-to-DNA ratio, and incubation time to achieve improved TE and increased gene expression levels.
CD38 restrains the activity of extracellular cGAMP in a model of multiple myeloma Lorenzo Cuollo, Samuele Di Cristofano, Annamaria Sandomenico, Emanuela Iaccarino, Angela Oliver, Alessandra Zingoni, Marco Cippitelli, Cinzia Fionda, Sara Petillo, Andrea Kosta, Valentina Tassinari, Maria Teresa Petrucci, Francesca Fazio, Menotti Ruvo, Angela Santoni, Domenico Raimondo, Alessandra Soriani Iscience, 2024 molecular modeling and cell-free biochemical assays to show a direct interaction between the catalytic pocket of CD38 and cGAMP. Altogether, our findings expand the current knowledge about the regulation of cGAMP activity.
NEDD8-activating enzyme inhibition potentiates the anti-myeloma activity of natural killer cells Sara Petillo, Elena Sproviero, Luisa Loconte, Lorenzo Cuollo, Alessandra Zingoni, Rosa Molfetta, Cinzia Fionda, Alessandra Soriani, Cristina Cerboni, Maria Teresa Petrucci, Francesca Fazio, Rossella Paolini, Angela Santoni, Marco Cippitelli Cell Death and Disease, 2023 Natural Killer (NK) cells act as important regulators in the development and progression of hematological malignancies and their suppressor activity against Multiple Myeloma (MM) cells has been confirmed in many studies. Significant changes in the distribution of NK cell subsets and dysfunctions of NK cell effector activities were described in MM patients and correlated with disease staging. Thus, restoring or enhancing the functionality of these effectors for the treatment of MM represents a critical need. Neddylation is a post-translational modification that adds a ubiquitin-like molecule, NEDD8, to the substrate protein. One of the outcomes is the activation of the Cullin Ring Ligases (CRLs), a class of ubiquitin-ligases that controls the degradation of about 20% of proteasome-regulated proteins. Overactivation of CRLs has been described in cancer and can lead to tumor growth and progression. Thus, targeting neddylation represents an attractive approach for cancer treatment. Our group has recently described how pharmacologic inhibition of neddylation increases the expression of the NKG2D activating receptor ligands, MICA and MICB, in MM cells, making these cells more susceptible to NK cell degranulation and killing. Here, we extended our investigation to the direct role of neddylation on NK cell effector functions exerted against MM. We observed that inhibition of neddylation enhanced NK cell-mediated degranulation and killing against MM cells and improved Daratumumab/Elotuzumab-mediated response. Mechanistically, inhibition of neddylation increased the expression of Rac1 and RhoA GTPases in NK cells, critical mediators for an efficient degranulation at the immunological synapse of cytotoxic lymphocytes, and augmented the levels of F-actin and perforin polarization in NK cells contacting target cells. Moreover, inhibition of neddylation partially abrogated TGFβ-mediated repression of NK cell effector activity. This study describes the role of neddylation on NK cell effector functions and highlights the positive immunomodulatory effects achieved by the inhibition of this pathway in MM.
When killers become thieves: Trogocytosed PD-1 inhibits NK cells in cancer M. S. Hasim, M. Marotel, Jonathan J. Hodgins, E. Vulpis, Olivia J Makinson, Sara Asif, Han-Yun Shih, Amit K Scheer, Olivia MacMillan, Felipe G Alonso, K. Burke, D. Cook, Rui Li, M. Petrucci, A. Santoni, P. Fallon, A. Sharpe, G. Sciumè, A. Veillette, A. Zingoni, D. Gray, A. McCurdy, M. Ardolino Science Advances, 2022
Opsonin-Deficient Nucleoproteic Corona Endows UnPEGylated Liposomes with Stealth Properties In Vivo Francesca Giulimondi, Elisabetta Vulpis, Luca Digiacomo, Maria Valeria Giuli, Angelica Mancusi, Anna Laura Capriotti, Aldo Laganà, Andrea Cerrato, Riccardo Zenezini Chiozzi, Carmine Nicoletti, Heinz Amenitsch, Francesco Cardarelli, Laura Masuelli, Roberto Bei, Isabella Screpanti, Daniela Pozzi, Alessandra Zingoni, Saula Checquolo, Giulio Caracciolo ACS Nano, 2022
Cereblon regulates NK cell cytotoxicity and migration via Rac1 activation Cinzia Fionda, Helena Stabile, Rosa Molfetta, Andrea Kosta, Giovanna Peruzzi, Silvia Ruggeri, Alessandra Zingoni, Cristina Capuano, Alessandra Soriani, Rossella Paolini, Angela Gismondi, Marco Cippitelli, Angela Santoni European Journal of Immunology, 2021
Immune complexes exposed on mast cell-derived nanovesicles amplify allergic inflammation Rosa Molfetta, Mario Lecce, Linda Quatrini, Giulio Caracciolo, Luca Digiacomo, Laura Masuelli, Nadia Domenica Milito, Elisabetta Vulpis, Alessandra Zingoni, Ricciarda Galandrini, Angela Santoni, Rossella Paolini Allergy European Journal of Allergy and Clinical Immunology, 2020
Tuning the Orchestra: HCMV vs. Innate Immunity Valentina Dell’Oste, Matteo Biolatti, Ganna Galitska, Gloria Griffante, Francesca Gugliesi, Selina Pasquero, Alessandra Zingoni, Cristina Cerboni, Marco De Andrea Frontiers in Microbiology, 2020
MICA-129 dimorphism and soluble MICA are associated with the progression of multiple myeloma Alessandra Zingoni, Elisabetta Vulpis, Francesca Cecere, Maria G. Amendola, Daniel Fuerst, Taron Saribekyan, Adnane Achour, Tatyana Sandalova, Ilaria Nardone, Agnese Peri, Alessandra Soriani, Cinzia Fionda, Elena Mariggiò, Maria T. Petrucci, Maria R. Ricciardi, Joannis Mytilineos, Marco Cippitelli, Cristina Cerboni, Angela Santoni Frontiers in Immunology, 2018
NKG2D and its ligands: "One for all, all for one" Alessandra Zingoni, Rosa Molfetta, Cinzia Fionda, Alessandra Soriani, Rossella Paolini, Marco Cippitelli, Cristina Cerboni, Angela Santoni Frontiers in Immunology, 2018
Molecular Cloning of TER1, a Chemokine Receptor-Like Gene Expressed by Lymphoid Tissues Journal of Immunology, 1996
Molecular cloning and expression of cDNA encoding the rat UDP-N-acetylglucosamine:α-6-D-mannoside β-1,2-N-acetylglucosaminyltransferase II Journal of Biological Chemistry, 1995
RECENT SCHOLAR PUBLICATIONS
Targeting RNA polymerase I to boost natural killer cell anticancer activity in multiple myeloma E Sproviero, E Gnocchini, T Cipollone, S Petillo, C Cassone, R Molfetta, ... Cell Death & Disease 16 (1), 865 , 2025 2025
ADAR1 expression is associated with cervical cancer progression and negatively regulates NK cell activity V Tassinari, M Kaciulis, S Petrai, H Stabile, A Pernazza, M Leopizzi, ... JCI insight 10 (13), e190244 , 2025 2025 Citations: 1
Precondensed Plasmid DNA Enhances CAR-T Cell Generation via Lipid Nanoparticles A Pirrottina, S Renzi, L Digiacomo, F Giulimondi, V De Lorenzi, S Ghignoli, ... ACS omega 10 (27), 29804-29814 , 2025 2025 Citations: 3
NKG2D triggering hampers DNAM-1-mediated signaling in human NK cells C Marangio, ND Milito, E Putro, A Carnevale, C Capuano, A Zingoni, ... Frontiers in Immunology 16, 1575059 , 2025 2025 Citations: 8
Protein‐DNA Competition at the Bio‐Nano Interface: Structural and Biological Insights From Graphene Oxide Coronas (Adv. Mater. Interfaces 6/2025). E Quagliarini, F Giulimondi, S Renzi, A Pirrottina, A Zingoni, N Carboni, ... Advanced Materials Interfaces 12 (6) , 2025 2025
Protein‐DNA Competition at the Bio‐Nano Interface: Structural and Biological Insights From Graphene Oxide Coronas E Quagliarini, F Giulimondi, S Renzi, A Pirrottina, A Zingoni, N Carboni, ... Advanced Materials Interfaces 12 (6), 2400560 , 2025 2025 Citations: 4
Structuring lipid nanoparticles, DNA, and protein corona into stealth bionanoarchitectures for in vivo gene delivery S Renzi, L Digiacomo, D Pozzi, E Quagliarini, E Vulpis, MV Giuli, ... Nature Communications 15 (1), 9119 , 2024 2024 Citations: 45
Exploiting the cGAS/STING pathway to revert the immunosuppressive environment of multiple myeloma and boost Natural Killer cell-mediated immunosurveillance C Cassone, E Gnocchini, E Sproviero, F Fazio, MT Petrucci, C Cerboni, ... EUROPEAN JOURNAL OF IMMUNOLOGY 54, 1076-1076 , 2024 2024
RNA Polymerase I Inhibition and activation of Nucleolar Stress Response in the anticancer activity of Natural Killer cells against Multiple Myeloma E Sproviero, T Cipollone, E Gnocchini, S Petillo, C Cassone, A Zingoni, ... EUROPEAN JOURNAL OF IMMUNOLOGY 54, 1077-1077 , 2024 2024
Optimizing transfection efficiency in CAR-T cell manufacturing through multiple administrations of lipid-based nanoparticles F Giulimondi, L Digiacomo, S Renzi, C Cassone, A Pirrottina, R Molfetta, ... ACS Applied Bio Materials 7 (6), 3746-3757 , 2024 2024 Citations: 16
CD38 restrains the activity of extracellular cGAMP in a model of multiple myeloma L Cuollo, S Di Cristofano, A Sandomenico, E Iaccarino, A Oliver, ... IScience 27 (5) , 2024 2024 Citations: 7
The senescence journey in cancer immunoediting A Zingoni, F Antonangeli, S Sozzani, A Santoni, M Cippitelli, A Soriani Molecular Cancer 23 (1), 68 , 2024 2024 Citations: 72
NEDD8-activating enzyme inhibition potentiates the anti-myeloma activity of natural killer cells S Petillo, E Sproviero, L Loconte, L Cuollo, A Zingoni, R Molfetta, ... Cell Death & Disease 14 (7), 438 , 2023 2023 Citations: 15
Cross-dressing of multiple myeloma cells mediated by extracellular vesicles conveying MIC and ULBP ligands promotes NK cell killing E Vulpis, L Loconte, C Cassone, F Antonangeli, G Caracciolo, L Masuelli, ... International Journal of Molecular Sciences 24 (11), 9467 , 2023 2023 Citations: 10
Doxorubicin–mediated miR–433 expression on exosomes promotes bystander senescence in multiple myeloma cells in a DDR–Independent manner E Vulpis, L Cuollo, C Borrelli, F Antonangeli, L Masuelli, M Cippitelli, ... International Journal of Molecular Sciences 24 (7), 6862 , 2023 2023 Citations: 13
Women in NK and innate lymphoid cell biology A Zingoni, T Bellon Frontiers in Immunology 14, 1157166 , 2023 2023
NKG2D engagement on human NK cells leads to DNAM‐1 hypo‐responsiveness through different converging mechanisms ND Milito, A Zingoni, H Stabile, A Soriani, C Capuano, M Cippitelli, ... European Journal of Immunology 53 (2), 2250198 , 2023 2023 Citations: 18
NKG2D down-modulation on human NK cells is followed by DNAM-1 hypo-responsivenss C Marangio, ND Milito, A Zingoni, H Stabile, A Soriani, C Capuano, ... XIV National SIICA Congress 2023 , 2023 2023
Rescue SLAMF7 activity in exhausted natural killer cells: Novel challenges in the immunotherapy of multiple myeloma A Zingoni, M Cippitelli Clinical and Translational Discovery 2 (4) , 2022 2022
GAS6/TAM signaling pathway controls MICA expression in multiple myeloma cells A Kosta, A Mekhloufi, L Lucantonio, A Zingoni, A Soriani, M Cippitelli, ... Frontiers in Immunology 13, 942640 , 2022 2022 Citations: 9
MOST CITED SCHOLAR PUBLICATIONS
ATM-ATR–dependent up-regulation of DNAM-1 and NKG2D ligands on multiple myeloma cells by therapeutic agents results in enhanced NK-cell susceptibility and is associated with a … A Soriani, A Zingoni, C Cerboni, ML Iannitto, MR Ricciardi, ... Blood, The Journal of the American Society of Hematology 113 (15), 3503-3511 , 2009 2009 Citations: 561
Cutting edge: the chemokine receptor CCR8 is preferentially expressed in Th2 but not Th1 cells A Zingoni, H Soto, JA Hedrick, A Stoppacciaro, CT Storlazzi, F Sinigaglia, ... The Journal of Immunology 161 (2), 547-551 , 1998 1998 Citations: 543
Antigen-activated human T lymphocytes express cell-surface NKG2D ligands via an ATM/ATR-dependent mechanism and become susceptible to autologous NK-cell lysis C Cerboni, A Zingoni, M Cippitelli, M Piccoli, L Frati, A Santoni Blood, The Journal of the American Society of Hematology 110 (2), 606-615 , 2007 2007 Citations: 378
Cross-Talk between Activated Human NK Cells and CD4 + T Cells via OX40-OX40 Ligand Interactions A Zingoni, T Sornasse, BG Cocks, Y Tanaka, A Santoni, LL Lanier The Journal of Immunology 173 (6), 3716-3724 , 2004 2004 Citations: 366
NKG2D and its ligands:“one for all, all for one” A Zingoni, R Molfetta, C Fionda, A Soriani, R Paolini, M Cippitelli, ... Frontiers in immunology 9, 476 , 2018 2018 Citations: 313
Aberrant in vivo T helper type 2 cell response and impaired eosinophil recruitment in CC chemokine receptor 8 knockout mice SW Chensue, NW Lukacs, TY Yang, X Shang, KA Frait, SL Kunkel, ... The Journal of experimental medicine 193 (5), 573-584 , 2001 2001 Citations: 292
Interplay of protein corona and immune cells controls blood residency of liposomes F Giulimondi, L Digiacomo, D Pozzi, S Palchetti, E Vulpis, AL Capriotti, ... Nature communications 10 (1), 3686 , 2019 2019 Citations: 273
Human immunodeficiency virus 1 Nef protein downmodulates the ligands of the activating receptor NKG2D and inhibits natural killer cell-mediated cytotoxicity C Cerboni, F Neri, N Casartelli, A Zingoni, D Cosman, P Rossi, A Santoni, ... Journal of general virology 88 (1), 242-250 , 2007 2007 Citations: 245
The DNA damage response: a common pathway in the regulation of NKG2D and DNAM-1 ligand expression in normal, infected, and cancer cells C Cerboni, C Fionda, A Soriani, A Zingoni, M Doria, M Cippitelli, ... Frontiers in immunology 4, 508 , 2014 2014 Citations: 184
Natural killer cell response to chemotherapy-stressed cancer cells: role in tumor immunosurveillance A Zingoni, C Fionda, C Borrelli, M Cippitelli, A Santoni, A Soriani Frontiers in immunology 8, 1194 , 2017 2017 Citations: 169
DNAM-1 ligand expression on Ag-stimulated T lymphocytes is mediated by ROS-dependent activation of DNA-damage response: relevance for NK–T cell interaction M Ardolino, A Zingoni, C Cerboni, F Cecere, A Soriani, ML Iannitto, ... Blood, The Journal of the American Society of Hematology 117 (18), 4778-4786 , 2011 2011 Citations: 167
Senescent cells: Living or dying is a matter of NK cells F Antonangeli, A Zingoni, A Soriani, A Santoni Journal of Leukocyte Biology 105 (6), 1275-1283 , 2019 2019 Citations: 154
Genotoxic stress modulates the release of exosomes from multiple myeloma cells capable of activating NK cell cytokine production: Role of HSP70/TLR2/NF-kB axis E Vulpis, F Cecere, R Molfetta, A Soriani, C Fionda, G Peruzzi, ... Oncoimmunology 6 (3), e1279372 , 2017 2017 Citations: 142
Exosome-delivered microRNAs promote IFN-α secretion by human plasmacytoid DCs via TLR7 V Salvi, V Gianello, S Busatto, P Bergese, L Andreoli, U D’Oro, A Zingoni, ... JCI insight 3 (10), e98204 , 2018 2018 Citations: 137
Engagement of NKG2D by Cognate Ligand or Antibody Alone Is Insufficient to Mediate Costimulation of Human and Mouse CD8 + T Cells LIR Ehrlich, K Ogasawara, JA Hamerman, R Takaki, A Zingoni, JP Allison, ... The Journal of Immunology 174 (4), 1922-1931 , 2005 2005 Citations: 133
NK cell regulation of T cell-mediated responses A Zingoni, T Sornasse, BG Cocks, Y Tanaka, A Santoni, LL Lanier Molecular immunology 42 (4), 451-454 , 2005 2005 Citations: 127
Multiple myeloma impairs bone marrow localization of effector natural killer cells by altering the chemokine microenvironment A Ponzetta, G Benigni, F Antonangeli, G Sciumè, E Sanseviero, A Zingoni, ... Cancer research 75 (22), 4766-4777 , 2015 2015 Citations: 125
Genotoxic stress induces senescence-associated ADAM10-dependent release of NKG2D MIC ligands in multiple myeloma cells A Zingoni, F Cecere, E Vulpis, C Fionda, R Molfetta, A Soriani, ... The Journal of Immunology 195 (2), 736-748 , 2015 2015 Citations: 124
Human leukocyte antigen E contributes to protect tumor cells from lysis by natural killer cells EL Monaco, E Tremante, C Cerboni, E Melucci, L Sibilio, A Zingoni, ... Neoplasia 13 (9), 822-IN14 , 2011 2011 Citations: 115
CD69‐triggered ERK activation and functions are negatively regulated by CD94/NKG2‐A inhibitory receptor A Zingoni, G Palmieri, S Morrone, M Carretero, M Lopez‐Botel, M Piccoli, ... European journal of immunology 30 (2), 644-651 , 2000 2000 Citations: 114