Single cell RNAseq signatures refined with combiroc enhance identification of NK cells in blood and solid tissues Ivan Ferrari, Saveria Mazzara, Andrea Gobbini, Noemi Di Marzo, Mariacristina Crosti, Sergio Abrignani, Renata Grifantini, Mauro Bombaci, Riccardo L. Rossi Scientific Reports, 2026 Cytotoxic CD8 T lymphocytes (CTLs) and natural killer (NK) cells share the common objective of controlling infections and detecting and removing tumor cells, albeit through distinct target recognition mechanisms. Although CTLs belong to the adaptive immune system and NK cells are innate lymphoid cells, they frequently exhibit considerable overlap in their molecular phenotypes. This overlap, as with many others in cell biology, poses challenges for distinguishing cells in the context of single cell transcriptomics. Building on a previous ROC-driven combinatorial approach, we developed a new computational framework for single-cell RNA-seq with the combiroc R package, and in this study we showed that it can identify non-canonical marker combinations for NK cells in Peripheral Blood Mononuclear Cell datasets. These combinatorial markers were in line with the Human Protein Atlas and we validated them through cytometry staining and functional assays. Markers selected with combiroc exhibit exceptional discriminatory power for identifying NK cells, both in blood and solid tumoral tissues. Besides this finding, we showed that our approach vastly optimizes standard differential expression signatures: it reduces dimensionality while improving interpretability and transferability to diagnostic applications, offering a practical solution for refining immune cell identities in complex transcriptomic datasets.
Autosomal Dominant Hyper-IgE Syndrome Patients Retain IL10-Producing preTh17-Cells That Are Activated by Opportunistic Pathogens and Support IgE Production Giorgia Moschetti, Chiara Vasco, Francesca Clemente, Paola Larghi, Sara Maioli, Edoardo Scarpa, Elena Carelli, Nadia Pulvirenti, Maria Lucia Sarnicola, Mariacristina Crosti, Manal Bel Imam, Willem van de Veen, Loris Rizzello, Sergio Abrignani, Lucia A. Baselli, Rosa Maria Dellepiane, Maria Carrabba, Giovanna Fabio, Jens Geginat Allergy European Journal of Allergy and Clinical Immunology, 2026 Background Autosomal Dominant‐Hyper‐IgE Syndrome (AD‐HIES) is caused by dominant‐negative (DN) STAT3 mutations and characterized by high IgE levels, a lack of Th17‐cells, and recurrent infections with extracellular pathogens. We previously identified an enigmatic population of IL‐10 producing CCR6 + B‐helper T‐cells and investigated here their relationship to Th17‐cells and STAT3 signaling requirements. Methods Human blood lymphocytes were analyzed by multiparametric flow cytometry in healthy donors and AD‐HIES patients. Analysis was performed by conventional gating or with bioinformatic tools. FACS‐purified T‐cell subsets were activated in vitro and Th17 differentiation assessed. T‐cell antigen specificities were assessed by activation with heat‐killed pathogens or antigenic peptide pools. B helper capacities were determined according to antibody secretion in B‐T co‐cultures by ELISA. Results CCR6 + Th‐cells that lacked subset‐defining differentiation markers (“CCR6 SP ”) were mostly non‐polarized central memory T‐cells (T CM ) that produced IL‐10 and expressed RORγt. They were pre‐committed to a Th17 fate, since TCR stimulation in the absence of polarizing cytokines induced efficient Th17 differentiation. The latter was promoted by an autocrine loop of STAT3‐activating cytokines. CCR6 + Th‐cells were reduced in patients with DN‐STAT3 mutations but contained activated CCR6 SP T‐cells that produced IL‐10 and responded vigorously to AD‐HIES‐associated pathogens. These residual CCR6 + Th‐cells provided B‐cell help for IgG and IgE production. Conclusions Th17 differentiation in AD‐HIES patients was not completely impaired but arrested at an intermediate stage of IL‐10‐producing “pre‐Th17”‐cells. Surprisingly, DN‐STAT3 mutations did not inhibit IL‐10 production by CD4 + T‐cells. Pre‐Th17‐cells were activated by AD‐HIES‐associated pathogens and possessed B‐helper functions, suggesting that they are not protective but may promote aberrant IgE production.
A human CAGinSTEM platform for decoding HTT repeats’ somatic instability links CAG interruption to HD pathology in neurons Martina Zobel, Gianluca Damaggio, Maria Lidia Mignogna, Dario Besusso, Davide Scalzo, Andrea Cossu, Camilla Trovesi, Mariacristina Crosti, Francesco Cortina, Ilaria Campus, Giulio Formenti, Saveria Mazzara, Francesco Gregoretti, Laura Antonelli, Gennaro Oliva, Chiara Zuccato, Vincenza Colonna, Paola Conforti, Matteo Cereda, Riccardo Lorenzo Rossi, Simone Maestri, Andrea Scolz, Raffale Iennaco, Elena Cattaneo Cell Reports, 2025 Somatic CAG instability in the mutant Huntingtin (HTT) gene is increasingly recognized as a key hallmark of Huntington's disease (HD). Using our novel human CAGinSTEM platform, we manipulated cis genetic elements influencing instability in human HD neurons, monitoring repeat length. Quality-controlled CRISPR-engineered stem cells with increasing CAG lengths and clinical haplotypes were analyzed using third-generation sequencing. Our findings link interruptions in the CAG repeat, especially the loss or duplication of the penultimate CAA of canonical alleles, to significant instability modulation. Notably, four internal CAA interruptions completely abolish CAG instability, reversing HD phenotypes such as altered striatal fate acquisition and nuclear disorganization. This platform highlights the role of cis modifiers, emphasizing the direct influence of HTT DNA repeat composition on CAG instability and providing a robust framework for modeling HTT repeat instability in vitro.
V-ATPase in glioma stem cells: a novel metabolic vulnerability Alessandra Maria Storaci, Irene Bertolini, Cristina Martelli, Giorgia De Turris, Nadia Mansour, Mariacristina Crosti, Maria Rosaria De Filippo, Luisa Ottobrini, Luca Valenti, Elisa Polledri, Silvia Fustinoni, Manuela Caroli, Claudia Fanizzi, Silvano Bosari, Stefano Ferrero, Giorgia Zadra, Valentina Vaira Journal of Experimental and Clinical Cancer Research, 2025 Background Glioblastoma (GBM) is a lethal brain tumor characterized by the glioma stem cell (GSC) niche. The V-ATPase proton pump has been described as a crucial factor in sustaining GSC viability and tumorigenicity. Here we studied how patients-derived GSCs rely on V-ATPase activity to sustain mitochondrial bioenergetics and cell growth. Methods V-ATPase activity in GSC cultures was modulated using Bafilomycin A1 (BafA1) and cell viability and metabolic traits were analyzed using live assays. The GBM patients-derived orthotopic xenografts were used as in vivo models of disease. Cell extracts, proximity-ligation assay and advanced microscopy was used to analyze subcellular presence of proteins. A metabolomic screening was performed using Biocrates p180 kit, whereas transcriptomic analysis was performed using Nanostring panels. Results Perturbation of V-ATPase activity reduces GSC growth in vitro and in vivo. In GSC there is a pool of V-ATPase that localize in mitochondria. At the functional level, V-ATPase inhibition in GSC induces ROS production, mitochondrial damage, while hindering mitochondrial oxidative phosphorylation and reducing protein synthesis. This metabolic rewiring is accompanied by a higher glycolytic rate and intracellular lactate accumulation, which is not exploited by GSCs for biosynthetic or survival purposes. Conclusions V-ATPase activity in GSC is critical for mitochondrial metabolism and cell growth. Targeting V-ATPase activity may be a novel potential vulnerability for glioblastoma treatment.
Chromatin remodeling restrains oncogenic functions in prostate cancer Valentina Rosti, Giovanni Lembo, Cristiano Petrini, Francesca Gorini, Roberto Quadri, Chiara Cordiglieri, Margherita Mutarelli, Elisa Salviato, Elisabetta Casari, Emanuele Di Patrizio Soldateschi, Emanuele Montanari, Giancarlo Albo, Francesco Ripa, Alessandra Fasciani, Mariacristina Crosti, Elisa De Lorenzis, Marco Maggioni, Valentina Vaira, Maria Vivo, Francesco Ferrari, Chiara Lanzuolo Nature Communications, 2025 Primary prostate cancer presents with multifocal lesions and unpredictable clinical behavior, posing significant challenges for effective prognosis. To address this, we investigate the epigenomic landscape of prostate tumor biopsies from 25 treatment-naïve male patients by analyzing chromatin compartmentalization patterns. Our analysis reveals two distinct molecular subtypes: one with a Low Degree of Decompartmentalization (LDD) and another with a High Degree of Decompartmentalization (HDD). Here we show that the HDD subgroup exhibits extensive chromatin reorganization associated with diminished oncogenic potential. This subtype shows repression of molecular pathways involved in extracellular matrix remodeling and cellular plasticity. From this distinction, we derive an 18-gene transcriptional signature capable of differentiating HDD from LDD cases. Importantly, we validate the prognostic relevance of this signature in multiple independent cohorts totaling over 900 patients. Our findings suggest that epigenetic-derived signature at the time of diagnostic biopsy can offer a powerful tool for risk stratification in prostate cancer. Prostate cancer (PCa) evaluation remains challenging due to its heterogenous and multifocal nature. Here, the authors reconstruct the nuclear chromatin compartmentalization of PCa patients-derived biopsies distinguishing two epigenetic subtypes and deriving an 18-gene signature with prognostic value on TCGA samples that is further validated with multiple independent PCa cohorts.
Transplanted human striatal progenitors exhibit functional integration and modulate host circuitry in a Huntington's disease animal model Linda Scaramuzza, Marta Ribodino, Christian Cassarino, Marta Morrocchi, Gabriela B Gomez Gonzalez, Roberta Parolisi, Edoardo Sozzi, Giacomo Turrini, Valentina Cerrato, Paola Conforti, Eriola Hoxha, Riccardo Tognato, Greta Galeotti, Chiara Cordiglieri, Maria Cristina Crosti, Stefano Zucca, Martina Lorenzati, Serena Bovetti, Paolo Spaiardi, Claudio de’Sperati, Gerardo Biella, Linda Ottoboni, Malin Parmar, Simone Maestri, Dario Besusso, Elena Cattaneo, Annalisa Buffo Pharmacological Research, 2025 Huntington's disease (HD) is a fatal neurodegenerative disorder caused by a CAG repeat expansion in the HTT gene. This leads to progressive loss of striatal neurons and motor-cognitive decline. While current gene-targeting approaches aiming at reducing somatic instability show promise - especially in case of early treatment - they cannot restore the already compromised neuronal circuitry at advanced disease stages. Thus, cell replacement therapy offers a regenerative strategy to rebuild damaged striatal circuits. Here, we report that human striatal progenitors (hSPs) derived from embryonic stem cells via a morphogen-guided protocol survive long-term when transplanted into a rodent model of HD and recapitulate key aspects of ventral telencephalic development. By employing single-nucleus RNAseq of the grafted cells, we resolved their transcriptional profile with unprecedented resolution. This has identified transcriptional signals of D1- and D2-type medium spiny neurons (MSN), Medial Ganglionic Eminence (MGE) and Caudal Ganglionic Eminence (CGE) -derived interneurons, and regionally specified astrocytes. Moreover, we demonstrate that grafted cells undergo further maturation 6 months post-transplantation, acquiring the expected regionally defined transcriptional identity. Immunohistochemistry confirmed stable graft composition over time and supported a neurogenic-to-gliogenic switch post-transplantation. Multiple complementary techniques including virus-based tracing and electrophysiology assays demonstrated anatomical and functional integration of the grafts. Notably, chemogenetic modulation of graft activity regulated striatal-dependent behaviors, further supporting effective graft integration into host basal ganglia circuits. Altogether, these results provide preclinical evidence that hSP-grafts can reconstruct striatal circuits and modulate functionally relevant behaviors. The ability to generate a scalable, molecularly defined progenitor population capable of in vivo functional integration supports the potential of hSPs for clinical application in HD and related basal ganglia disorders.
The Human Bone Marrow May Offer an IL-15-Dependent Survival Niche for EOMES+ Tr1-Like Cells Nadia Pulvirenti, Chiara Vasco, Camilla Righetti, Petra Dadova, Giacomo Boffa, Alice Laroni, Tiziana Vigo, Anna Maria Raiola, Maria Cristina Crosti, Stefano Maglie, Luca Valenti, Daniele Prati, Sergio Abrigani, Antonio Uccelli, Jens Geginat European Journal of Immunology, 2025 Maintenance of memory T‐cells in the bone marrow and systemically depends on the homeostatic cytokines IL‐7 and IL‐15. An immunological memory may also exist for regulatory T‐cells. EOMES+type‐1 regulatory (Tr1)‐like cells have a rapid in vivo turnover, but whether they are short‐lived effector cells or are maintained long‐term has not been investigated.EOMES+Tr1‐like cells expressing GzmK were enriched among CD69+Ki67−T‐cells in the bone marrow of healthy donors, suggesting that they became quiescent and bone marrow‐resident. Conversely, CD4+GzmB+ effector T‐cells were excluded from the bone marrow‐resident fraction. The dichotomy between GzmK+ and GzmB+T‐cells was observed both in healthy individuals and in multiple sclerosis patients, and also among CD8+T‐cells. Intriguingly, bone marrow‐resident CD4+ memory T‐cells expressed increased levels of IL‐7Rα, while EOMES+Tr1‐like cells were consistently IL‐7Rαlo. However, EOMES+Tr1‐like cells expressed the IL‐2/15Rβ chain, and the latter was induced upon forced expression of EOMES in primary human CD4+ T‐cells. Finally, IL‐15 rescued EOMES+Tr1‐enriched populations from death by neglect but was not required for CD4+ memory T‐cell survival. These findings suggest that the bone marrow may provide a survival niche for EOMES+Tr1‐like cells. The different IL‐7 and IL‐15 receptor expression patterns of CD4+ memory T‐cells and EOMES+Tr1‐like cells suggest furthermore that they compete for different homeostatic niches.
Generation of Human 3D Airway Assembloids for Advanced Modeling Maria Chiara Iachini, Alberto Coglot, Dorian Tace, Noemi Elia, Francesco Rusconi, Federica Cosentino, Gianluca Lopez, Mariacristina Crosti, Tuğba Dursun Usal, Edoardo Scarpa, Antonio D'Amore, Vitale Miceli, Lorenzo Rosso, Lorenza Lazzari International Journal of Biological Sciences, 2025 The development of physiologically relevant in vitro 3D models is crucial for studying lung biology and disease mechanisms. While airway organoids have significantly improved our ability to mimic lung tissue, they lack key nonepithelial components that are essential for tissue homeostasis. Here, we describe the generation of human airway assembloids, combining airway organoids, stromal fibroblasts, and endothelial cells to better replicate the native lung environment. The model was generated from healthy lung tissue donors by using a scaffold-free culture system to promote cell self-organization. Assembloids exhibited long-term viability, maintained typical airway epithelial markers, and demonstrated functional characteristics, such as mucus production and ciliary beating. This technology provides a powerful platform for studying airway physiology, disease mechanisms, and therapeutic approaches, with potential applications in regenerative and personalized medicine. Our study established a novel, reproducible 3D assembloid model of the human airways, bridging the gap between traditional organoid cultures and complex tissue engineering strategies.
Reduced spike specific T-cell responses in COVID-19 vaccinated subjects undergoing SARS-CoV-2 breakthrough infection Stefania Varchetta, Federica Sole Golfetto, Patrizia Bono, Annapaola Callegaro, Tanya Fabbris, Andrea Favalli, Mariacristina Crosti, Tullia Maria De Feo, Nathalie Iannotti, Giorgio Bozzi, Valeria Castelli, Bianca Mariani, Antonio Muscatello, Sergio Abrignani, Renata Grifantini, Alessandra Bandera, Andrea Lombardi Frontiers in Immunology, 2025 IntroductionT-cell responses to SARS-CoV-2 remain largely preserved across variants despite waning neutralizing antibodies. However, T-cell immunity may vary with the host’s immune status, and data on T-cell responses in post-vaccine infections (PVI) are limited.MethodsWe assessed Spike-specific T-cell responses in 32 vaccinated individuals, 16 of whom experienced PVI. Immune responses were evaluated at three time points: 1 month after the second vaccine dose (T1), 1 month after the booster dose (T2), and, in the PVI group, 1–3 months after the first positive nasal swab (T3). Additionally, we evaluated anti-spike antibody levels, T-cell exhaustion markers, and natural killer cell subsets, focusing on memory-like CD57+ NKG2C+ cells.ResultsSubjects who developed PVI exhibited significantly reduced Spike-specific CD4 T-cell responses following the booster dose compared to vaccinated individuals who remained uninfected. This was accompanied by increased frequencies of LAG-3+ CD4+ and CD8+ T-cells. A positive correlation was observed between AIM+ CD4+ T-cells and NKG2C+ NK cells at T2 in PVI subjects. Following natural infection, T-cell responses were enhanced and associated with an expansion of NKG2C+ NK cells.ConclusionsIndividuals experiencing PVI displayed impaired booster-induced CD4+ T-cell responses and increased expression of the immune checkpoint LAG-3. Natural infection restored and enhanced cellular immunity, particularly through the expansion of Spike-specific T-cells and memory NK cell populations. This study identifies an immune profile characterized by low spike-specific responses, which are associated with an increased susceptibility to breakthrough infections.
LINE1 modulate human T cell function by regulating protein synthesis during the life span Filippo V. Burattin, Rebecca Vadalà, Michele Panepuccia, Valeria Ranzani, Mariacristina Crosti, Federico A. Colombo, Cristina Ruberti, Elisa Erba, Daniele Prati, Teresa Nittoli, Giovanni Montini, Andrea Ronchi, Lorenza Pugni, Fabio Mosca, Sara Ricciardi, Sergio Abrignani, Carlo Pietrasanta, Federica Marasca, Beatrice Bodega Science Advances, 2024
Corrigendum: TMEM123 a key player in immune surveillance of colorectal cancer (Frontiers in Immunology, (2023), 14, (1194087), 10.3389/fimmu.2023.1194087) Elisa Pesce, Chiara Cordiglieri, Mauro Bombaci, Serenella Eppenberger-Castori, Stefania Oliveto, Cristina Manara, Mariacristina Crosti, Caner Ercan, Mairene Coto, Andrea Gobbini, Susanna Campagnoli, Tiziano Donnarumma, Manuele Martinelli, Valeria Bevilacqua, Elisa De Camilli, Paola Gruarin, Maria L. Sarnicola, Elisa Cassinotti, Ludovica Baldari, Giuseppe Viale, Stefano Biffo, Sergio Abrignani, Luigi M. Terracciano, Renata Grifantini Frontiers in Immunology, 2023
TMEM123 a key player in immune surveillance of colorectal cancer Elisa Pesce, Chiara Cordiglieri, Mauro Bombaci, Serenella Eppenberger-Castori, Stefania Oliveto, Cristina Manara, Mariacristina Crosti, Caner Ercan, Mairene Coto, Andrea Gobbini, Susanna Campagnoli, Tiziano Donnarumma, Manuele Martinelli, Valeria Bevilacqua, Elisa De Camilli, Paola Gruarin, Maria L. Sarnicola, Elisa Cassinotti, Ludovica Baldari, Giuseppe Viale, Stefano Biffo, Sergio Abrignani, Luigi M. Terracciano, Renata Grifantini Frontiers in Immunology, 2023
Fate mapping and scRNA sequencing reveal origin and diversity of lymph node stromal precursors Elisa Lenti, Luca Genovese, Silvia Bianchessi, Aurora Maurizio, Simona Baghai Sain, Alessia di Lillo, Greta Mattavelli, Itamar Harel, Francesca Bernassola, Thomas Hehlgans, Klaus Pfeffer, Mariacristina Crosti, Sergio Abrignani, Sylvia M. Evans, Giovanni Sitia, Nuno Guimarães-Camboa, Vincenzo Russo, Serge A. van de Pavert, Jose Manuel Garcia-Manteiga, Andrea Brendolan Immunity, 2022
LINE1 are spliced in non-canonical transcript variants to regulate T cell quiescence and exhaustion Federica Marasca, Shruti Sinha, Rebecca Vadalà, Benedetto Polimeni, Valeria Ranzani, Elvezia Maria Paraboschi, Filippo Vittorio Burattin, Marco Ghilotti, Mariacristina Crosti, Maria Luce Negri, Susanna Campagnoli, Samuele Notarbartolo, Andrea Sartore-Bianchi, Salvatore Siena, Daniele Prati, Giovanni Montini, Giuseppe Viale, Olga Torre, Sergio Harari, Renata Grifantini, Giulia Soldà, Stefano Biffo, Sergio Abrignani, Beatrice Bodega Nature Genetics, 2022
Maturation signatures of conventional dendritic cell subtypes in COVID-19 suggest direct viral sensing Laura Marongiu, Giulia Protti, Fabio A. Facchini, Mihai Valache, Francesca Mingozzi, Valeria Ranzani, Anna Rita Putignano, Lorenzo Salviati, Valeria Bevilacqua, Serena Curti, Mariacristina Crosti, Maria Lucia Sarnicola, Mariella D'Angiò, Laura Rachele Bettini, Andrea Biondi, Luca Nespoli, Nicolò Tamini, Nicola Clementi, Nicasio Mancini, Sergio Abrignani, Roberto Spreafico, Francesca Granucci European Journal of Immunology, 2022
Inositol 1,4,5-trisphosphate 3-kinase B promotes Ca2+mobilization and the inflammatory activity of dendritic cells Laura Marongiu, Francesca Mingozzi, Clara Cigni, Roberta Marzi, Marco Di Gioia, Massimiliano Garrè, Dario Parazzoli, Laura Sironi, Maddalena Collini, Reiko Sakaguchi, Takashi Morii, Mariacristina Crosti, Monica Moro, Stéphane Schurmans, Tiziano Catelani, Rany Rotem, Miriam Colombo, Stephen Shears, Davide Prosperi, Ivan Zanoni, Francesca Granucci Science Signaling, 2021
Evidence for a pathogenic role of extrafollicular, IL-10-producing CCR6 + B helper T cells in systemic lupus erythematosus F. Facciotti, P. Larghi, R. Bosotti, C. Vasco, N. Gagliani, C. Cordiglieri, S. Mazzara, V. Ranzani, E. Rottoli, S. Curti, A. Penatti, B. Karnani, Y. Kobayashi, M. Crosti, M. Bombaci, J. P. van Hamburg, G. Rossetti, R. Gualtierotti, M. Gerosa, S. Gatti, S. Torretta, L. Pignataro, S. W. Tas, S. Abrignani, M. Pagani, F. Grassi, P. L. Meroni, R. A. Flavell, J. Geginat Proceedings of the National Academy of Sciences of the United States of America, 2020
Eomesodermin controls a unique differentiation program in human IL-10 and IFN-γ coproducing regulatory T cells Paola Gruarin, Stefano Maglie, Marco De Simone, Barbara Häringer, Chiara Vasco, Valeria Ranzani, Roberto Bosotti, Johanna S. Noddings, Paola Larghi, Federica Facciotti, Maria L. Sarnicola, Martina Martinovic, Mariacristina Crosti, Monica Moro, Riccardo L. Rossi, Maria E. Bernardo, Flavio Caprioli, Franco Locatelli, Grazisa Rossetti, Sergio Abrignani, Massimiliano Pagani, Jens Geginat European Journal of Immunology, 2019
FGF2 and EGF Are Required for Self-Renewal and Organoid Formation of Canine Normal and Tumor Breast Stem Cells Cinzia Cocola, Stefano Molgora, Eleonora Piscitelli, Maria Cristina Veronesi, Marianna Greco, Cinzia Bragato, Monica Moro, Mariacristina Crosti, Brian Gray, Luciano Milanesi, Valeria Grieco, Gaia Cecilia Luvoni, James Kehler, Gianfranco Bellipanni, Rolland Reinbold, Ileana Zucchi, Antonio Giordano Journal of Cellular Biochemistry, 2017
Extracellular MicroRNA signature of human helper T cell subsets in health and autoimmunity Anna Torri, Donatella Carpi, Elisabetta Bulgheroni, Maria-Cristina Crosti, Monica Moro, Paola Gruarin, Riccardo L. Rossi, Grazisa Rossetti, Dolores Di Vizio, Mirjam Hoxha, Valentina Bollati, Cristina Gagliani, Carlo Tacchetti, Moira Paroni, Jens Geginat, Laura Corti, Luigia Venegoni, Emilio Berti, Massimiliano Pagani, Giuseppe Matarese, Sergio Abrignani, Paola de Candia Journal of Biological Chemistry, 2017
Transcriptional Landscape of Human Tissue Lymphocytes Unveils Uniqueness of Tumor-Infiltrating T Regulatory Cells Marco De Simone, Alberto Arrigoni, Grazisa Rossetti, Paola Gruarin, Valeria Ranzani, Claudia Politano, Raoul J.P. Bonnal, Elena Provasi, Maria Lucia Sarnicola, Ilaria Panzeri, Monica Moro, Mariacristina Crosti, Saveria Mazzara, Valentina Vaira, Silvano Bosari, Alessandro Palleschi, Luigi Santambrogio, Giorgio Bovo, Nicola Zucchini, Mauro Totis, Luca Gianotti, Giancarlo Cesana, Roberto A. Perego, Nirvana Maroni, Andrea Pisani Ceretti, Enrico Opocher, Raffaele De Francesco, Jens Geginat, Hendrik G. Stunnenberg, Sergio Abrignani, Massimiliano Pagani Immunity, 2016
IL-10-producing forkhead box protein 3-negative regulatory T cells inhibit B-cell responses and are involved in systemic lupus erythematosus Federica Facciotti, Nicola Gagliani, Barbara Häringer, Johanna Sophie Alfen, Alessandra Penatti, Stefano Maglie, Moira Paroni, Andrea Iseppon, Monica Moro, Maria Cristina Crosti, Katharina Stölzel, Chiara Romagnani, Gabriella Moroni, Francesca Ingegnoli, Sara Torretta, Lorenzo Pignataro, Andrea Annoni, Fabio Russo, Massimiliano Pagani, Sergio Abrignani, Pierluigi Meroni, Richard Flavell, Jens Geginat Journal of Allergy and Clinical Immunology, 2016
Intracellular Modulation, Extracellular Disposal and Serum Increase of MiR-150 Mark Lymphocyte Activation Paola de Candia, Anna Torri, Tatiana Gorletta, Maya Fedeli, Elisabetta Bulgheroni, Cristina Cheroni, Francesco Marabita, Mariacristina Crosti, Monica Moro, Elena Pariani, Luisa Romanò, Susanna Esposito, Fabio Mosca, Grazisa Rossetti, Riccardo L. Rossi, Jens Geginat, Giulia Casorati, Paolo Dellabona, Massimiliano Pagani, Sergio Abrignani Plos One, 2013
Human CD1c+ dendritic cells secrete high levels of IL-12 and potently prime cytotoxic T-cell responses Giulia Nizzoli, Jana Krietsch, Anja Weick, Svenja Steinfelder, Federica Facciotti, Paola Gruarin, Annalisa Bianco, Bodo Steckel, Monica Moro, Mariacristina Crosti, Chiara Romagnani, Katharina Stölzel, Sara Torretta, Lorenzo Pignataro, Carmen Scheibenbogen, Petra Neddermann, Raffaele De Francesco, Sergio Abrignani, Jens Geginat Blood, 2013
Identification of new autoantigens by protein array indicates a role for IL4 neutralization in autoimmune hepatitis Chiara Zingaretti, Milena Arigò, Angela Cardaci, Monica Moro, Mariacristina Crosti, Antonella Sinisi, Elisa Sugliano, Cristina Cheroni, Francesco Marabita, Renzo Nogarotto, Raoul Jean Pierre Bonnal, Paolo Marcatili, Maurizio Marconi, Annalinda Zignego, Paolo Muratori, Pietro Invernizzi, Piero Colombatto, Maurizia Brunetto, Ferruccio Bonino, Raffaele De Francesco, Jens Geginat, Massimiliano Pagani, Luigi Muratori, Sergio Abrignani, Mauro Bombaci Molecular and Cellular Proteomics, 2012
CD4+ T Cells from Healthy Subjects and Colon Cancer Patients Recognize a Carcinoembryonic Antigen-specific Immunodominant Epitope Cancer Research, 2003
