Stefano Mantero

@article{pmid31938717,

title = {Generation of an immunodeficient mouse model of tcirg1-deficient autosomal recessive osteopetrosis},

author = {E Palagano and S Muggeo and L Crisafulli and I L Tourkova and D Strina and S Mantero and E Fontana and S L Locatelli and M Monari and E Morenghi and C Carlo-Stella and J B Barnett and H C Blair and P Vezzoni and A Villa and C Sobacchi and F Ficara},

year  = {2020},

date = {2020-06-01},

journal = {Bone Rep},

volume = {12},

pages = {100242},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid32099849,

title = {Chromosome Ŧransplantation: A Possible Approach to Ŧreat Ħuman X-linked Đisorders},

author = {M Paulis and L Susani and A Castelli and T Suzuki and T Hara and L Straniero and S Duga and D Strina and S Mantero and E Caldana and L S Sergi and A Villa and P Vezzoni},

year  = {2020},

date = {2020-06-01},

journal = {Mol Ther Methods Clin Dev},

volume = {17},

pages = {369--377},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31295380,

title = {Absence of Đipeptidyl Peptidase 3 Increases Oxidative Stress and Causes Bone Loss},

author = {C Menale and L J Robinson and E Palagano and R Rigoni and M Erreni and A J Almarza and D Strina and S Mantero and M Lizier and A Forlino and R Besio and M Monari and P Vezzoni and B Cassani and H C Blair and A Villa and C Sobacchi},

year  = {2019},

date = {2019-01-01},

journal = {J Bone Miner Res},

volume = {34},

number = {11},

pages = {2133--2148},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid30184340,

title = {Mesenchymal Stromal Cell-Seeded Biomimetic Scaffolds as a Factory of Soluble RANKL in Rankl-Đeficient Osteopetrosis},

author = {C Menale and E Campodoni and E Palagano and S Mantero and M Erreni and A Inforzato and E Fontana and F Schena and R Van't Hof and M Sandri and A Tampieri and A Villa and C Sobacchi},

year  = {2019},

date = {2019-01-01},

journal = {Stem Cells Transl Med},

volume = {8},

number = {1},

pages = {22--34},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29105104,

title = {B lymphocytes limit senescence-driven fibrosis resolution and favor hepatocarcinogenesis in mouse liver injury},

author = {F Faggioli and E Palagano and L Di Tommaso and M Donadon and V Marrella and C Recordati and S Mantero and A Villa and P Vezzoni and B Cassani},

year  = {2018},

date = {2018-01-01},

journal = {Hepatology},

volume = {67},

number = {5},

pages = {1970--1985},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29421274,

title = {Autonomous role of Wiskott-Aldrich syndrome platelet deficiency in inducing autoimmunity and inflammation},

author = {L Sereni and M C Castiello and F Marangoni and A Anselmo and D di Silvestre and S Motta and E Draghici and S Mantero and A J Thrasher and S Giliani and A Aiuti and P Mauri and L D Notarangelo and M Bosticardo and A Villa},

year  = {2018},

date = {2018-01-01},

journal = {J Allergy Clin Immunol},

volume = {142},

number = {4},

pages = {1272--1284},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29929043,

title = {Mutations in the Neuroblastoma Amplified Sequence gene in a family affected by Acrofrontofacionasal Đysostosis type 1},

author = {E Palagano and G Zuccarini and P Prontera and R Borgatti and G Stangoni and S Elisei and S Mantero and C Menale and A Forlino and P Uva and M Oppo and P Vezzoni and A Villa and G R Merlo and C Sobacchi},

year  = {2018},

date = {2018-01-01},

journal = {Bone},

volume = {114},

pages = {125--136},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29558369,

title = {UĦRF1 epigenetically orchestrates smooth muscle cell plasticity in arterial disease},

author = {L Elia and P Kunderfranco and P Carullo and M Vacchiano and F M Farina and I F Hall and S Mantero and C Panico and R Papait and G Condorelli and M Quintavalle},

year  = {2018},

date = {2018-01-01},

journal = {J Clin Invest},

volume = {128},

number = {6},

pages = {2473--2486},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{lizier_fusion_2016,

title = {Fusion between cancer cells and macrophages occurs in a murine model of spontaneous neu+ breast cancer without increasing its metastatic potential},

author = {Michela Lizier and Achille Anselmo and Stefano Mantero and Francesca Ficara and Marianna Paulis and Paolo Vezzoni and Franco Lucchini and Giovanni Pacchiana},

doi = {10.18632/oncotarget.11508},

issn = {1949-2553},

year  = {2016},

date = {2016-09-01},

journal = {Oncotarget},

volume = {7},

number = {38},

pages = {60793--60806},

abstract = {Cell fusion between neoplastic and normal cells has been suggested to play a role in the acquisition of a malignant phenotype. Several studies have pointed to the macrophage as the normal partner in this fusion, suggesting that the fused cells could acquire new invasive properties and become able to disseminate to distant organs. However, this conclusion is mainly based on studies with transplantable cell lines. We tested the occurrence of cell fusion in the MMTV-neu model of mouse mammary carcinoma. In the first approach, we generated aggregation chimeras between GFP/neu and RFP/neu embryos. Tumor cells would display both fluorescent proteins only if cell fusion with normal cells occurred. In addition, if cell fusion conferred a growth/dissemination advantage, cells with both markers should be detectable in lung metastases at increased frequency. We confirmed that fused cells are present at low but consistent levels in primary neoplasms and that the macrophage is the normal partner in the fusion events. Similar results were obtained using a second approach in which bone marrow from mice carrying the Cre transgene was transplanted into MMTV-neu/LoxP-tdTomato transgenic animals, in which the Tomato gene is activated only in the presence of CRE recombinase. However, no fused cells were detected in lung metastases in either model. We conclude that fusion between macrophages and tumor cells does not confer a selective advantage in our spontaneous model of breast cancer, although these data do not rule out a possible role in models in which an inflammation environment is prominent.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{rigoni_intestinal_2016,

title = {Intestinal microbiota sustains inflammation and autoimmunity induced by hypomorphic RAG defects},

author = {Rosita Rigoni and Elena Fontana and Simone Guglielmetti and Bruno Fosso and Anna Maria D'Erchia and Virginia Maina and Valentina Taverniti and Maria Carmina Castiello and Stefano Mantero and Giovanni Pacchiana and Silvia Musio and Rosetta Pedotti and Carlo Selmi and Rodrigo J Mora and Graziano Pesole and Paolo Vezzoni and Pietro Luigi Poliani and Fabio Grassi and Anna Villa and Barbara Cassani},

doi = {10.1084/jem.20151116},

issn = {1540-9538},

year  = {2016},

date = {2016-03-01},

journal = {The Journal of Experimental Medicine},

volume = {213},

number = {3},

pages = {355--375},

abstract = {Omenn syndrome (OS) is caused by hypomorphic Rag mutations and characterized by a profound immunodeficiency associated with autoimmune-like manifestations. Both in humans and mice, OS is mediated by oligoclonal activated T and B cells. The role of microbial signals in disease pathogenesis is debated. Here, we show that Rag2(R229Q) knock-in mice developed an inflammatory bowel disease affecting both the small bowel and colon. Lymphocytes were sufficient for disease induction, as intestinal CD4 T cells with a Th1/Th17 phenotype reproduced the pathological picture when transplanted into immunocompromised hosts. Moreover, oral tolerance was impaired in Rag2(R229Q) mice, and transfer of wild-type (WT) regulatory T cells ameliorated bowel inflammation. Mucosal immunoglobulin A (IgA) deficiency in the gut resulted in enhanced absorption of microbial products and altered composition of commensal communities. The Rag2(R229Q) microbiota further contributed to the immunopathology because its transplant into WT recipients promoted Th1/Th17 immune response. Consistently, long-term dosing of broad-spectrum antibiotics (ABXs) in Rag2(R229Q) mice ameliorated intestinal and systemic autoimmunity by diminishing the frequency of mucosal and circulating gut-tropic CCR9(+) Th1 and Th17 T cells. Remarkably, serum hyper-IgE, a hallmark of the disease, was also normalized by ABX treatment. These results indicate that intestinal microbes may play a critical role in the distinctive immune dysregulation of OS.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}