7 results on '"Roncelin, S."'
Search Results
2. Pitfalls in anti-influenza T cell detection by Elispot using thimerosal containing pandemic H1N1 vaccine as antigen
- Author
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Chauvat, A., primary, Benhamouda, N., additional, Loison, E., additional, Gougeon, M.L., additional, Gey, A., additional, Levionnois, E., additional, Ravel, P., additional, Abitbol, V., additional, Roncelin, S., additional, Marcheteau, E., additional, Quintin-Colonna, F., additional, Fridman, W.H., additional, Launay, O., additional, and Tartour, E., additional
- Published
- 2012
- Full Text
- View/download PDF
3. Soluble interleukin-2 receptor and metalloproteinase-9 expression in head and neck cancer: prognostic value and analysis of their relationships
- Author
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El Houda Agueznay, N, primary, Badoual, C, additional, Hans, S, additional, Gey, A, additional, Vingert, B, additional, Peyrard, S, additional, Quintin-Colonna, F, additional, Ravel, P, additional, Bruneval, P, additional, Roncelin, S, additional, Lelongt, B, additional, Bertoglio, J, additional, Fridman, W H, additional, Brasnu, D, additional, and Tartour, E, additional
- Published
- 2007
- Full Text
- View/download PDF
4. Rare germline complement factor H variants in patients with paroxysmal nocturnal hemoglobinuria.
- Author
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Prata PH, Galimard JE, Sicre de Fontbrune F, Duval A, Vieira Martins P, Roncelin S, Debureaux PÉ, Lepretre AC, Larcher L, Birsen R, Benhamou Y, Soulier J, Socié G, Fremeaux-Bacchi V, and Peffault de Latour R
- Subjects
- Humans, Anemia, Aplastic, Hemolysis, Complement Factor H genetics, Hemoglobinuria, Paroxysmal drug therapy, Hemoglobinuria, Paroxysmal genetics, Thrombosis
- Abstract
Patients with paroxysmal nocturnal hemoglobinuria (PNH) are susceptible to complement-mediated intravascular hemolysis and thrombosis. Factor H (FH) is the main regulator of the complement alternative pathway, which protects cells from unwanted complement-mediated damage. Although FH is not a glycosylphosphatidylinositol-linked molecule, it may play a role in PNH. We sought to determine if rare germline variants in complement factor H (CFH) affect the PNH course, screening 84 patients with PNH treated with eculizumab for rare variants in CFH, CFI, and C3 genes. We compared the allelic frequencies with populational data and a geographically-matched control group, looking for an association between presence of the variants and treatment response (transfusion independence by 6 months). Sixteen patients presented rare variants, 9 in CFH (10.7%). Germline CFH variants were more frequent among patients with PNH than among controls (P = .02) or public data (P < .001) and were more likely to be transfusion-dependent at 6 months after eculizumab initiation (P = .015). With a median follow-up of 5.8 years, 8 of 9 patients with the CFH variant received transfusions, and 2 developed thromboses. None of the patients with the CFH variant had severe aplastic anemia from eculizumab initiation until 6 months. We demonstrated for the first time that rare CFH variants are over-represented among patients with PNH and that germline genetic background may affect the response to eculizumab., (© 2023 by The American Society of Hematology.)
- Published
- 2023
- Full Text
- View/download PDF
5. Assessing complement blockade in patients with paroxysmal nocturnal hemoglobinuria receiving eculizumab.
- Author
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Peffault de Latour R, Fremeaux-Bacchi V, Porcher R, Xhaard A, Rosain J, Castaneda DC, Vieira-Martins P, Roncelin S, Rodriguez-Otero P, Plessier A, Sicre de Fontbrune F, Abbes S, Robin M, and Socié G
- Subjects
- Adult, Aged, Antibodies, Monoclonal, Humanized blood, Antibodies, Monoclonal, Humanized therapeutic use, Bilirubin blood, Biomarkers blood, Complement Activation drug effects, Complement C5 metabolism, Erythrocyte Transfusion, Female, Hemoglobinuria, Paroxysmal blood, Hemoglobinuria, Paroxysmal immunology, Hemoglobinuria, Paroxysmal pathology, Hemolysis drug effects, Hemolysis immunology, Humans, Immunoassay, Immunologic Factors blood, Immunologic Factors therapeutic use, Infusions, Intravenous, L-Lactate Dehydrogenase blood, Male, Middle Aged, Antibodies, Monoclonal, Humanized pharmacokinetics, Complement C5 antagonists & inhibitors, Drug Monitoring methods, Hemoglobinuria, Paroxysmal drug therapy, Immunologic Factors pharmacokinetics
- Abstract
Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by intravascular hemolysis, which is effectively controlled with eculizumab, a humanized monoclonal antibody that binds complement protein 5 (C5). The residual functional activity of C5 can be screened using a 50% hemolytic complement (CH50) assay, which is sensitive to the reduction, absence, and/or inactivity of any components of the classical and terminal complement pathway. Little data exist on complement blockade during treatment. From 2010 to 2012, clinical data, hemolysis biomarkers, complement assessment, and free eculizumab circulating levels were systematically measured immediately before every injection given to 22 patients with hemolytic PNH while receiving eculizumab therapy. During the study, 6 patients received ≥1 red blood cell transfusion. Lack of detectable CH50 activity (defined by CH50 ≤ 10% of normal values) was found in 184 samples (51%) and was significantly associated with lower lactate dehydrogenase levels (P = .002). Low levels of circulating free eculizumab (<50 µg/mL) correlated with detectable CH50 activity (CH50 > 10%; P = .004), elevated bilirubin levels (P < .0001), and the need for transfusions (P = .034). This study suggests that both CH50 activity and circulating free eculizumab levels may help physicians to manage PNH patients receiving eculizumab., (© 2015 by The American Society of Hematology.)
- Published
- 2015
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6. [Complement deficiencies and human diseases].
- Author
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Rosain J, Ngo S, Bordereau P, Poulain N, Roncelin S, Vieira Martins P, Dragon-Durey MA, and Frémeaux-Bacchi V
- Subjects
- Autoimmune Diseases immunology, Bacterial Infections immunology, Complement Activation immunology, Complement System Proteins immunology, Disease Susceptibility immunology, Humans, Immunologic Deficiency Syndromes immunology, Complement System Proteins deficiency
- Abstract
The complement system is a complex system involving serum and membrane proteins interacting in a regulated manner. The complement system plays a major role in antibacterial immunity, in inflammation, and in immune complex processing. Therefore, deficiencies in complement proteins are associated with increased susceptibility to bacterial infections and autoimmune diseases. These deficiencies can be inherited or acquired. Most of them can be screened by simple laboratory tests but require a diagnosis in a specialized laboratory. All sequences of complement genes are known, and the discovery of a deficiency must lead to genetic testing. The discovery of a congenital deficiency requires a familial study and a prophylaxis. In this article, we review the complement cascade, the laboratory tests to explore it, and the main diseases associated with complement deficiencies.
- Published
- 2014
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7. A decrease of regulatory T cells correlates with overall survival after sunitinib-based antiangiogenic therapy in metastatic renal cancer patients.
- Author
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Adotevi O, Pere H, Ravel P, Haicheur N, Badoual C, Merillon N, Medioni J, Peyrard S, Roncelin S, Verkarre V, Mejean A, Fridman WH, Oudard S, and Tartour E
- Subjects
- Adenocarcinoma, Clear Cell immunology, Adenocarcinoma, Clear Cell mortality, Adenocarcinoma, Clear Cell physiopathology, Adenocarcinoma, Clear Cell secondary, Angiogenesis Inhibitors administration & dosage, Angiogenesis Inhibitors adverse effects, Antibodies, Monoclonal administration & dosage, Antibodies, Monoclonal adverse effects, Antibodies, Monoclonal, Humanized, Bevacizumab, Cell Count, Disease Progression, Disease-Free Survival, Female, Follow-Up Studies, Forkhead Transcription Factors biosynthesis, Humans, Indoles administration & dosage, Indoles adverse effects, Kidney Neoplasms immunology, Kidney Neoplasms mortality, Kidney Neoplasms pathology, Kidney Neoplasms physiopathology, Lung Neoplasms immunology, Lung Neoplasms mortality, Lung Neoplasms physiopathology, Lung Neoplasms secondary, Male, Neoadjuvant Therapy, Pyrroles administration & dosage, Pyrroles adverse effects, Sunitinib, Survival Analysis, T-Lymphocytes, Regulatory immunology, T-Lymphocytes, Regulatory metabolism, T-Lymphocytes, Regulatory pathology, Adenocarcinoma, Clear Cell drug therapy, Antineoplastic Combined Chemotherapy Protocols, Kidney Neoplasms drug therapy, Lung Neoplasms drug therapy, T-Lymphocytes, Regulatory drug effects
- Abstract
Sunitinib, an antiangiogenic molecule, is one of the first-line standard of care in the treatment of patients with metastatic renal cell carcinoma. However, it only benefits to a subgroup of patients and no predictive markers of sunitinib efficacy have been identified. Twenty-eight metastatic renal cell carcinomas were treated with sunitinib-based therapy and another subgroup of 7 primary renal cell cancer patients were also treated by sunitinib in a neoadjuvant trial. Measurements of CD3+CD4+CD25(hi) Foxp3+ regulatory T cells, an immunosuppressive cell population, were performed before and after each cycle of treatment in blood and tumor in a prospective study. We observed a decrease in the number of peripheral blood Foxp3+ regulatory T cells after each cycle of sunitinib-based therapy. The overall survival was significantly longer in patients showing a decrease in the number of Foxp3+ regulatory T cells after 2 or 3 cycles of treatment (P<0.05). The decrease in the number of regulatory T cells positively correlated with their number at baseline (P<0.01), but not with modification of tumor volume defined by Response Evaluation Criteria in Solid Tumors criteria. The clinical relevance of these results was also supported by an intratumoral decrease of regulatory T cells in 5 out of 7 patients treated by sunitinib in a neoadjuvant trial. Our study represents the first work reporting that the measurement of regulatory T cells may have a predictive value on antiangiogenic response. Antiangiogenic therapy also reversed immunosuppression in the tumor microenvironment which provides novel argument in human to favor its combination with immunotherapy.
- Published
- 2010
- Full Text
- View/download PDF
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