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Your search keyword '"Cimaz, R"' showing total 11 results
Start Over Author "Cimaz, R" Journal international journal of immunopathology and pharmacology
11 results on '"Cimaz, R"'

1. Anti-TNF Agents as Therapeutic Choice in Immune-Mediated Inflammatory Diseases: Focus on Adalimumab

Author

Armuzzi, A., primary, Lionetti, P., additional, Blandizzi, C., additional, Caporali, R., additional, Chimenti, S., additional, Cimino, L., additional, Gionchetti, P., additional, Girolomoni, G., additional, Lapadula, G., additional, Marchesoni, A., additional, Marcellusi, A., additional, Mennini, F.S., additional, Salvarani, C., additional, and Cimaz, R., additional

Published
2014
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2. The Role of Tumour Necrosis Factor in the Pathogenesis of Immune-Mediated Diseases

Author

Blandizzi, C., primary, Gionchetti, P., additional, Armuzzi, A., additional, Caporali, R., additional, Chimenti, S., additional, Cimaz, R., additional, Cimino, L., additional, Lapadula, G., additional, Lionetti, P., additional, Marchesoni, A., additional, Marcellusi, A., additional, Mennini, F.S., additional, Salvarani, C., additional, and Girolomoni, G., additional

Published
2014
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3. Adalimumab in the Treatment of Immune-Mediated Diseases

Author

Lapadula, G., primary, Marchesoni, A., additional, Armuzzi, A., additional, Blandizzi, C., additional, Caporali, R., additional, Chimenti, S., additional, Cimaz, R., additional, Cimino, L., additional, Gionchetti, P., additional, Girolomoni, G., additional, Lionetti, P., additional, Marcellusi, A., additional, Mennini, F.S., additional, and Salvarani, C., additional

Published
2014
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6. Validation of a Diagnostic Score for the Diagnosis of Autoinflammatory Diseases in Adults

Author

Cantarini, L., primary, Iacoponi, F., additional, Lucherini, O.M., additional, Obici, L., additional, Brizi, M.G., additional, Cimaz, R., additional, Rigante, D., additional, Benucci, M., additional, Sebastiani, G.D., additional, Brucato, A., additional, Sabadini, L., additional, Simonini, G., additional, Giani, T., additional, Pasini, F. Laghi, additional, Baldari, C.T., additional, Bellisai, F., additional, Valentini, G., additional, Bombardieri, S., additional, Paolazzi, G, additional, and Galeazzi, M., additional

Published
2011
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10. Increased Percentages of Tumor Necrosis Factor-a+/Interferon-T+Lymphocytes and Calprotectin+/Tumor Necrosis Factor-A+ Monocytes in Patients with Acute Kawasaki Disease

Author

Guggino, G., Cimaz, R., Accomando, S., Pagnini, I., Simonini, G., Di Liberto, D., De Martino, M., Dieli, F., and Sireci, G.

Abstract

In vivoexposure to microorganisms resident in the oral cavity is considered as a possible cause of Kawasaki disease (KD), and some epitopes derived from streptococci display homology with Factor H of Complement. Additionally, calprotectin, a major calcium binding protein released by neutrophils and activated monocytes, could be directly involved in endothelial damage occurring in KD. The aim of our study is to evaluate the percentages of IFN-?+and/or TNF-a+lymphocytes and double positive calprotectin/TNF-a monocytes (CD14+) after in vitrostimulation with streptococcal- and/or Factor H-derived peptides, in patients with acute KD. Peripheral Blood Mononuclear Cells (PBMCs) obtained from KD patients and febrile controls were stimulated in vitrowith peptides. After culture, cells were collected, stained with fluorochrome-labelled monoclonal antibodies against CD3, CD14, calprotectin, IFN-? and TNF-a, and cytofluorimetric analyses were performed. Our results showed increased percentages of TNF-a+/IFN-?+lymphocytes in KD patients in respect to controls when PBMCs were stimulated with streptococcal or Factor H-derived epitopes. In addition, also calprotectin+/TNF-a+monocytes from KD patients were activated after PBMC in vitrostimulation. These findings lead us to speculate that some peptides, derived from oral streptococci and cross-reactive with the human Factor H of Complement, could induce lymphocyte and monocyte activation potentially involved in the pathogenesis of KD. Our results should be confirmed by further studies enrolling more patients and controls than those analyzed in our study.

Published
2012
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11. Increased percentages of tumor necrosis factor-alpha+/interferon-gamma+ T [corrected] lymphocytes and calprotectin+/tumor necrosis factor-alpha+ monocytes in patients with acute Kawasaki disease.

Author

Guggino G, Cimaz R, Accomando S, Pagnini I, Simonini G, Di Liberto D, De Martino M, Dieli F, and Sireci G

Subjects
Acute Disease, Cells, Cultured, Child, Female, Humans, Lipopolysaccharide Receptors physiology, Male, Interferon-gamma blood, Leukocyte L1 Antigen Complex blood, Monocytes chemistry, Mucocutaneous Lymph Node Syndrome immunology, T-Lymphocytes chemistry, Tumor Necrosis Factor-alpha blood
Abstract

In vivo exposure to microorganisms resident in the oral cavity is considered as a possible cause of Kawasaki disease (KD), and some epitopes derived from streptococci display homology with Factor H of Complement. Additionally, calprotectin, a major calcium binding protein released by neutrophils and activated monocytes, could be directly involved in endothelial damage occurring in KD. The aim of our study is to evaluate the percentages of IFN-gamma+ and/or TNF-alpha+ lymphocytes and double positive calprotectin/TNF-alpha monocytes (CD14+) after in vitro stimulation with streptococcal- and/or Factor H-derived peptides, in patients with acute KD. Peripheral Blood Mononuclear Cells (PBMCs) obtained from KD patients and febrile controls were stimulated in vitro with peptides. After culture, cells were collected, stained with fluorochrome-labelled monoclonal antibodies against CD3, CD14, calprotectin, IFN-gamma and TNF-alpha, and cytofluorimetric analyses were performed. Our results showed increased percentages of TNF-alpha+/IFN-gamma+ lymphocytes in KD patients in respect to controls when PBMCs were stimulated with streptococcal or Factor H-derived epitopes. In addition, also calprotectin+/TNF-alpha+ monocytes from KD patients were activated after PBMC in vitro stimulation. These findings lead us to speculate that some peptides, derived from oral streptococci and cross-reactive with the human Factor H of Complement, could induce lymphocyte and monocyte activation potentially involved in the pathogenesis of KD. Our results should be confirmed by further studies enrolling more patients and controls than those analyzed in our study.

Published
2012
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