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Your search keyword '"de Paulis, Amato"' showing total 11 results
Start Over Author "de Paulis, Amato" Journal frontiers in immunology
11 results on '"de Paulis, Amato"'

1. Risk for cancer development in familial Mediterranean fever and associated predisposing factors: an ambidirectional cohort study from the international AIDA Network registries

Author

Vitale, Antonio, primary, Caggiano, Valeria, additional, Tufan, Abdurrahman, additional, Ragab, Gaafar, additional, Batu, Ezgi Deniz, additional, Portincasa, Piero, additional, Aragona, Emma, additional, Sota, Jurgen, additional, Conti, Giovanni, additional, De Paulis, Amato, additional, Rigante, Donato, additional, Olivieri, Alma Nunzia, additional, Şahin, Ali, additional, La Torre, Francesco, additional, Lopalco, Giuseppe, additional, Cattalini, Marco, additional, Maggio, Maria Cristina, additional, Insalaco, Antonella, additional, Sfikakis, Petros P., additional, Verrecchia, Elena, additional, Yildirim, Derya, additional, Kucuk, Hamit, additional, Kardas, Riza Can, additional, Laymouna, Ahmed Hatem, additional, Ghanema, Mahmoud, additional, Saad, Moustafa Ali, additional, Sener, Seher, additional, Ercan Emreol, Hulya, additional, Ozen, Seza, additional, Jaber, Nour, additional, Khalil, Mohamad, additional, Di Ciaula, Agostino, additional, Gaggiano, Carla, additional, Malizia, Giuseppe, additional, Affronti, Andrea, additional, Patroniti, Serena, additional, Romeo, Meri, additional, Sbalchiero, Jessica, additional, Della Casa, Francesca, additional, Mormile, Ilaria, additional, Silvaroli, Sara, additional, Gicchino, Maria Francesca, additional, Çelik, Neşe Çabuk, additional, Tarsia, Maria, additional, Karamanakos, Anastasios, additional, Hernández-Rodríguez, José, additional, Parronchi, Paola, additional, Opris-Belinski, Daniela, additional, Barone, Patrizia, additional, Recke, Andreas, additional, Costi, Stefania, additional, Sfriso, Paolo, additional, Giardini, Henrique A. Mayrink, additional, Gentileschi, Stefano, additional, Wiesik-Szewczyk, Ewa, additional, Vasi, Ibrahim, additional, Loconte, Roberta, additional, Jahnz-Różyk, Karina, additional, Martín-Nares, Eduardo, additional, Torres-Ruiz, Jiram, additional, Cauli, Alberto, additional, Conforti, Alessandro, additional, Emmi, Giacomo, additional, Li Gobbi, Francesca, additional, Biasi, Giovanni Rosario, additional, Terribili, Riccardo, additional, Ruscitti, Piero, additional, Del Giudice, Emanuela, additional, Tharwat, Samar, additional, Brucato, Antonio Luca, additional, Ogunjimi, Benson, additional, Hinojosa-Azaola, Andrea, additional, Balistreri, Alberto, additional, Fabiani, Claudia, additional, Frediani, Bruno, additional, and Cantarini, Luca, additional

Published
2024
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6. Is There a Role for Basophils in Cancer?

Author

Marone, Giancarlo, primary, Schroeder, John T., additional, Mattei, Fabrizio, additional, Loffredo, Stefania, additional, Gambardella, Adriana Rosa, additional, Poto, Remo, additional, de Paulis, Amato, additional, Schiavoni, Giovanna, additional, and Varricchi, Gilda, additional

Published
2020
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9. N-Formyl Peptide Receptors Induce Radical Oxygen Production in Fibroblasts Derived From Systemic Sclerosis by Interacting With a Cleaved Form of Urokinase Receptor

Author

Napolitano, Filomena, primary, Rossi, Francesca Wanda, additional, Pesapane, Ada, additional, Varricchio, Silvia, additional, Ilardi, Gennaro, additional, Mascolo, Massimo, additional, Staibano, Stefania, additional, Lavecchia, Antonio, additional, Ragno, Pia, additional, Selleri, Carmine, additional, Marone, Gianni, additional, Matucci-Cerinic, Marco, additional, de Paulis, Amato, additional, and Montuori, Nunzia, additional

Published
2018
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10. IgG Autoantibodies Against IgE from Atopic Dermatitis Can Induce the Release of Cytokines and Proinflammatory Mediators from Basophils and Mast Cells

Author

Remo Poto, Isabella Quinti, Gianni Marone, Maurizio Taglialatela, Amato de Paulis, Vincenzo Casolaro, Gilda Varricchi, Poto, Remo, Quinti, Isabella, Marone, Gianni, Taglialatela, Maurizio, de Paulis, Amato, Casolaro, Vincenzo, and Varricchi, Gilda

Subjects
Interleukin-13, Allergy, Immunology, Anti-IgE, Atopic dermatitis, Basophils, Mast cells, Animals, Autoantibodies, Cytokines, Eicosanoids, Histamine, Humans, Immunoglobulin E, Immunoglobulin G, Interleukin-4, Leukotriene C4, Prostaglandins, Rabbits, Dermatitis, Atopic, Immunology and Allergy
Abstract

IgE-mediated release of proinflammatory mediators and cytokines from basophils and mast cells is a central event in allergic disorders. Several groups of investigators have demonstrated the presence of autoantibodies against IgE and/or FcεRI in patients with chronic spontaneous urticaria. By contrast, the prevalence and functional activity of anti-IgE autoantibodies in atopic dermatitis (AD) are largely unknown. We evaluated the ability of IgG anti-IgE from patients with AD to induce thein vitroIgE-dependent activation of human basophils and skin and lung mast cells. Different preparations of IgG anti-IgE purified from patients with AD and rabbit IgG anti-IgE were compared for their triggering effects on thein vitrorelease of histamine and type 2 cytokines (IL-4, IL-13) from basophils and of histamine and lipid mediators (prostaglandin D2and cysteinyl leukotriene C4) from human skin and lung mast cells. One preparation of human IgG anti-IgE out of six patients with AD induced histamine release from basophils, skin and lung mast cells. This preparation of human IgG anti-IgE induced the secretion of cytokines and eicosanoids from basophils and mast cells, respectively. Human monoclonal IgE was a competitive antagonist of both human and rabbit IgG anti-IgE. Human anti-IgE was more potent than rabbit anti-IgE for IL-4 and IL-13 production by basophils and histamine, prostaglandin D2and leukotriene C4release from mast cells. Functional anti-IgE autoantibodies rarely occur in patients with AD. When present, they induce the release of proinflammatory mediators and cytokines from basophils and mast cells, thereby possibly contributing to sustained IgE-dependent inflammation in at least a subset of patients with this disorder.

Published
2022
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11. N-Formyl Peptide Receptors Induce Radical Oxygen Production in Fibroblasts Derived From Systemic Sclerosis by Interacting With a Cleaved Form of Urokinase Receptor

Author

Filomena Napolitano, Francesca Wanda Rossi, Ada Pesapane, Silvia Varricchio, Gennaro Ilardi, Massimo Mascolo, Stefania Staibano, Antonio Lavecchia, Pia Ragno, Carmine Selleri, Gianni Marone, Marco Matucci-Cerinic, Amato de Paulis, Nunzia Montuori, Napolitano, Filomena, Rossi, Francesca Wanda, Pesapane, Ada, Varricchio, Silvia, Ilardi, Gennaro, Mascolo, Massimo, Staibano, Stefania, Lavecchia, Antonio, Ragno, Pia, Selleri, Carmine, Marone, Gianni, Matucci-Cerinic, Marco, de Paulis, Amato, and Montuori, Nunzia

Subjects
lcsh:Immunologic diseases. Allergy, 0301 basic medicine, MAPK/ERK pathway, Fibrosi, systemic sclerosis, integrin, Integrin, Immunology, FPRs, RAC1, 03 medical and health sciences, Systemic sclerosi, 0302 clinical medicine, fibroblasts, medicine, Immunology and Allergy, Receptor, Fibroblast, skin and connective tissue diseases, Original Research, NADPH oxidase, biology, Chemistry, fibrosis, Chemotaxis, ROS, Cell biology, Urokinase receptor, Fibroblasts, Fibrosis, Inflammation, Systemic sclerosis, UPAR, 030104 developmental biology, medicine.anatomical_structure, inflammation, 030220 oncology & carcinogenesis, biology.protein, FPR, lcsh:RC581-607, uPAR
Abstract

Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by fibrosis, alteration in the microvasculature and immunologic abnormalities. It has been hypothesized that an abnormal redox state could regulate the persistent fibrotic phenotype in SSc patients. N-Formyl peptide receptors (FPRs) are chemotactic receptors overexpressed in fibroblasts derived from SSc patients. In this study, we demonstrated that stimulation of FPRs promotes the generation of reactive oxygen species (ROS) in skin fibroblasts. In fibroblast cells, ROS production was due to FPRs interaction with the urokinase receptor (uPAR) and to β1 integrin engagement. FPRs cross-talk with uPAR and integrins led to Rac1 and ERKs activation. FPRs stimulation increased gp91phox and p67phox expression as well as the direct interaction between GTP-Rac1 and p67phox, thus promoting assembly and activation of the NADPH oxidase complex. FPRs functions occur through interaction with a specific domain of uPAR (residues 88SRSRY92) that can be exposed on the cell membrane by protease-mediated receptor cleavage. Immunohistochemistry analysis with a specific anti-SRSRY antibody showed increased expression of uPAR in a cleaved form, which exposes the SRSRY sequence at its N-terminus (DIIDIII-uPAR88–92) in skin biopsies from SSc patients. As expected by the increased expression of both FPRs and DII-DIII-uPAR88-92, fibroblasts derived from SSc patients showed a significantly increase in ROS generation both at a basal level than after FPRs stimulation, as compared to fibroblasts from normal subjects. C37, a small molecule blocking the interaction between FPRs and uPAR, and selumetinib, a clinically approved MAPKK/ERK inhibitor, significantly inhibited FPRs-mediated ROS production in fibroblasts derived from SSc patients. Thus, FPRs, through the interaction with the uPA/uPAR system, can induce ROS generation in fibroblasts by activating the NADPH oxidase, playing a role in the alteration of the redox state observed in SSc.

Published
2018

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