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Start Over Author "Serio Bianca" Publisher american society of hematology
23 results on '"Serio Bianca"'

1. Hemopoiesis and Immune Cell Perturbations during Venetoclax Plus Azacytidine Treatment in Acute Myeloid Leukemia

Author

Giudice, Valentina, primary, Ferrara, Idalucia, additional, Gorrese, Marisa, additional, D'Alto, Francesca, additional, Guariglia, Roberto, additional, Luponio, Serena, additional, Pezzullo, Luca, additional, Mettivier, Laura, additional, Bertolini, Angela, additional, D'Addona, Matteo, additional, De Novellis, Danilo, additional, Cuffa, Bianca, additional, Serio, Bianca, additional, and Selleri, Carmine, additional

Published
2021
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2. Low-Density Granulocytes Are Decreased in Acute Myeloid Leukemia and in Myelodysplastic Syndromes with Negative Prognostic Factors

Author

Giudice, Valentina, primary, Gorrese, Marisa, additional, Ferrara, Idalucia, additional, Pepe, Rita, additional, Bertolini, Angela, additional, Vitolo, Rosa, additional, Marcucci, Rossella, additional, Manzo, Paola, additional, D'Addona, Matteo, additional, Martorelli, Maria Carmen, additional, Buonanno, Maria Teresa, additional, Langella, Maddalena, additional, Serio, Bianca, additional, and Selleri, Carmine, additional

Published
2021
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3. How to Improve the Definition of Chronic Lymphocytic Leukemia Outcome Using a Simple Flow Cytometric Score Based on CD49d and Homing Marker Expression

Author

Giudice, Valentina, primary, Rocco, Monia, additional, Pezzullo, Luca, additional, Villani, Giancarlo, additional, Rosamilio, Rosa, additional, Marino, Luigi, additional, Annunziata, Silvana, additional, Fontana, Raffaele, additional, Ferrara, Idalucia, additional, Serio, Bianca, additional, and Selleri, Carmine, additional

Published
2016
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7. Complement fraction 3 binding on erythrocytes as additional mechanism of disease in paroxysmal nocturnal hemoglobinuria patients treated by eculizumab

Author

Risitano, Antonio M., primary, Notaro, Rosario, additional, Marando, Ludovica, additional, Serio, Bianca, additional, Ranaldi, Danilo, additional, Seneca, Elisa, additional, Ricci, Patrizia, additional, Alfinito, Fiorella, additional, Camera, Andrea, additional, Gianfaldoni, Giacomo, additional, Amendola, Angela, additional, Boschetti, Carla, additional, Di Bona, Eros, additional, Fratellanza, Giorgio, additional, Barbano, Filippo, additional, Rodeghiero, Francesco, additional, Zanella, Alberto, additional, Iori, Anna Paola, additional, Selleri, Carmine, additional, Luzzatto, Lucio, additional, and Rotoli, Bruno, additional

Published
2009
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8. Permissive Conditions for Evolution of PNH Clones Are Characterized by Overproduction of IFN-γ by Clonal CD4 and CD8 T Cells, Fas-L by CTLs, and Promoted by Immunogenetic Background

Author

Clemente, Michael, primary, Cazzolli, Heather, primary, Jankowska, Anna, primary, O’Keefe, Christine, primary, Serio, Bianca, primary, Nyland, Susan, primary, Wlodarski, Marcin, primary, Epling-Burnette, PK, primary, Loughran, Thomas, primary, List, Alan, primary, Paquette, Ronald, primary, and Maciejewski, Jaroslaw, primary

Published
2008
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9. Subcutaneous Alemtuzumab Is a Safe and Effective Treatment for Global or Single-Lineage Immune-Mediated Marrow Failures: a Survey from the EBMT-WPSAA

Author

Risitano, Antonio M., primary, Seneca, Elisa, primary, Marando, Ludovica, primary, Serio, Bianca, primary, Selleri, Carmine, primary, Scalia, Giulia, primary, Vecchio, Luigi Del, primary, Iori, Annapaola, primary, Kulagin, Alexander, primary, Maury, Sebastien, primary, Halter, Joerg, primary, Gupta, Vikas, primary, Bacigalupo, Andrea, primary, Socié, Gerard, primary, Tichelli, Andre, primary, Marsh, Judith, primary, Schrezenmeier, Hubert, primary, Passweg, Jakob R., primary, and Rotoli, Bruno, primary

Published
2008
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10. C3-Mediated Extravascular Hemolysis as Additional Mechanism of Disease in Paroxysmal Nocturnal Hemoglobinuria (PNH) Patients Treated by the Complent Inhibitor Eculizumab

Author

Risitano, Antonio M., primary, Marando, Ludovica, primary, Ranaldi, Danilo, primary, Seneca, Elisa, primary, Serio, Bianca, primary, Gianfaldoni, Giacomo, primary, Antonioli, Elisabetta, primary, Milano, Filippo, primary, Amendola, Angela, primary, Boschetti, Carla, primary, Barcellini, Wilma, primary, Di Bona, Eros, primary, Carella, Angelo Michele, primary, Barbano, Filippo, primary, Bonfigli, Silvana, primary, Capalbo, Silvana, primary, Fabbiano, Francesco, primary, Pulini, Stefano, primary, Marino, Antonio, primary, Pietrogrande, Francesco, primary, Iuliano, Franco, primary, Rodeghiero, Francesco, primary, Zanella, Alberto, primary, Iori, Annapaola, primary, Notaro, Rosario, primary, Luzzatto, Lucio, primary, and Rotoli, Bruno, primary

Published
2008
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21. Analysis of Immunogenetic Factors in Paroxysmal Nocturnal Hemoglobinuria Reveal Increased Frequency of IL-10 Low Secretor Genotype and Correlates with Induced IL-10 Production

Author

Giridharan Ramsingh, Serio Bianca, Antonio M. Risitano, Zachary P. Nearman, Jaroslaw P. Maciejewski, and Chris Hung

Subjects
Immunology, Context (language use), Single-nucleotide polymorphism, Cell Biology, Hematology, Human leukocyte antigen, Immunogenetics, Biology, medicine.disease, Biochemistry, Interleukin 10, hemic and lymphatic diseases, Genotype, Paroxysmal nocturnal hemoglobinuria, medicine, Cytotoxic T cell
Abstract

Aplastic anemia (AA) and paroxysmal nocturnal hemoglobinuria (PNH) have a common pathogenesis related to an immune attack on hematopoietic progenitor and stem cells. While the inciting events are not known, it is possible that complex immunogenetic predisposition factors exist which, in the context of exogenous influences, determine risk for these diseases. They include HLA background, KIR genotype, cytokine and immunomodulatory gene polymorphisms as well as gene variants involved in peptide processing and presentation. We have empirically selected a number of important polymorphisms that were described in the context of various immunologic diseases and studied their frequency in a large cohort (N=57) of PNH patients. As binding of KIR to the appropriate HLA ligand (KIR-L) can modulate activation of Nk-cells and cytotoxic T lymphocytes, we examined the combined impact of KIR/KIR-L genotypes on the risk of PNH and PNH/AA syndrome. PNH showed a decreased frequency of inhibitory KIR-2DL1 and KIR-2DL3 genes (79% vs. 95%, p=.0054; 67% vs. 89%, p=.0032). Analysis of the KIR genotype in correlation with the corresponding KIR-L profile, deduced from HLA typing, revealed an increased frequency of unopposed 2DS2 (2DS2/C1 type, 37% vs.10%, p=.012) and 2DL2 (2DL2/C1 mismatch 37% vs 11%, p=.031) but these mismatches have a potentially opposing functional effect. Using sequence-specific PCR amplification and/or direct sequencing, we have genotyped DNA samples derived from our cohort who presented with different subtypes of PNH and studied single nucleotide polymorphisms (SNPs) in cytokine genes such as TNF-a (−308 G/A), TGF-b 1 (C/T codon 10, C/G codon 25), IL-10 (−1082 G/A), and IFN-g (+874 A/T) and immunomodulatory receptor genes like CTLA-4 exon 6 (+49 G/A), FcγRIIIa (158 F/V) and CD45-exons 6 (+138 A/G), and 4 (+54 A/G, +77 C/G). These SNPs are responsible for intrinsic differences in cytokine production and receptor function and can thereby influence immune physiologic and pathologic responses. PNH patients showed a significantly higher frequency of A/A polymorphisms at intron −1082 of the IL-10 gene consistent with a “low secretor phenotype” (36% PNH (N=50) vs 13.8% controls (N=363), p=0.0001). In contrast to a few smaller studies, no association with any other SNP tested was found. To establish whether this finding translates into functional consequences, we examined basal and PMA-induced IL-10 secretion in PNH patients andcontrols. Upon induction, IL-10 production increased in controls (N=5, 14.11± 9.8), while in general, stimulation resulted in a much weaker IL-10 response in PNH patients (N=6, 4.51± 2.16). However, when compared genotypic IL-10 “low secretors” (−1082 A/A) among PNH patients showed significantly lower induction levels of IL-10 (N=2, 3.1± 1.58) as compared to PNH patients with “normal/high secretor” genotypes (−1082 A/G,G/G) ((N=4, 5.22 +/−3.1). The low secretor IL-10 genotype may correspond to the exaggerated TH1 response in PNH and in general supports the notion that complex inherited traits may exist that genetically determine propensity to PNH evolution.

Published
2006
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23. Involvement of the urokinase-type plasminogen activator receptor in hematopoietic stem cell mobilization

Author

Pia Ragno, Patrizia Ricci, Nunzia Montuori, Guido Rossi, Carmine Selleri, Francesco Blasi, Bianca Serio, Maria Vincenza Carriero, Bruno Rotoli, Valeria Visconte, Nicolai Sidenius, C., Selleri, Montuori, Nunzia, P., Ricci, V., Visconte, M. V., Carriero, N., Sideniu, Serio, Bianca, F., Blasi, Rotoli, Bruno, Rossi, Guido, and P., Ragno

Subjects
medicine.medical_specialty, Sialic Acid Binding Ig-like Lectin 3, Immunology, Lipopolysaccharide Receptors, Antigens, Differentiation, Myelomonocytic, Receptors, Cell Surface, Biochemistry, CXCR4, Receptors, Urokinase Plasminogen Activator, Antigens, CD, Cell Movement, Internal medicine, Granulocyte Colony-Stimulating Factor, medicine, Humans, Progenitor cell, Hematopoietic Stem Cell Mobilization, Chemistry, uPAR, hematopoietic stem cell, Hematopoietic stem cell, Cell Biology, Hematology, Hematopoietic Stem Cells, Receptors, Formyl Peptide, Tissue Donors, Up-Regulation, Urokinase receptor, Haematopoiesis, Endocrinology, medicine.anatomical_structure, SuPAR, Cancer research, Stem cell
Abstract

We investigated the involvement of the urokinase-type plasminogen-activator receptor (uPAR) in granulocyte–colony-stimulating factor (G-CSF)–induced mobilization of CD34+ hematopoietic stem cells (HSCs) from 16 healthy donors. Analysis of peripheral blood mononuclear cells (PBMNCs) showed an increased uPAR expression after G-CSF treatment in CD33+ myeloid and CD14+ monocytic cells, whereas mobilized CD34+ HSCs remained uPAR negative. G-CSF treatment also induced an increase in serum levels of soluble uPAR (suPAR). Cleaved forms of suPAR (c-suPAR) were released in vitro by PBMNCs and were also detected in the serum of G-CSF–treated donors. c-suPAR was able to chemoattract CD34+ KG1 leukemia cells and CD34+ HSCs, as documented by their in vitro migratory response to a chemotactic suPAR-derived peptide (uPAR84-95). uPAR84-95 induced CD34+ KG1 and CD34+ HSC migration by activating the high-affinity fMet-Leu-Phe (fMLP) receptor (FPR). In addition, uPAR84-95 inhibited CD34+ KG1 and CD34+ HSC in vitro migration toward the stromal-derived factor 1 (SDF1), thus suggesting the heterologous desensitization of its receptor, CXCR4. Finally, uPAR84-95 treatment significantly increased the output of clonogenic progenitors from long-term cultures of CD34+ HSCs. Our findings demonstrate that G-CSF–induced upregulation of uPAR on circulating CD33+ and CD14+ cells is associated with increased uPAR shedding, which leads to the appearance of serum c-suPAR. c-suPAR could contribute to the mobilization of HSCs by promoting their FPR-mediated migration and by inducing CXCR4 desensitization.

Published
2005
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