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1. De novo germline mutation in the dual specificity phosphatase 10 gene accelerates autoimmune diabetes

Author

Foray, Anne-Perrine, Candon, Sophie, Hildebrand, Sara, Marquet, Cindy, Valette, Fabrice, Pecquet, Coralie, Lemoine, Sebastien, Langa-Vives, Francina, Dumas, Michael, Hu, Peipei, Santamaria, Pere, You, Sylvaine, Lyon, Stephen, Scott, Lindsay, Bu, Chun Hui, Wang, Tao, Xu, Darui, Moresco, Eva Marie Y., Scazzocchio, Claudio, Bach, Jean-François, Beutler, Bruce, and Chatenoud, Lucienne

Published
2021

4. Evaluation of T Cell Response to SARS-CoV-2 in Kidney Transplant Recipients Receiving Monoclonal Antibody Prophylaxis and the Utility of a Bivalent mRNA Vaccine Booster Dose

Author

Bertrand, Dominique, primary, Laurent, Charlotte, additional, Lemoine, Mathilde, additional, Lebourg, Ludivine, additional, Hanoy, Mélanie, additional, Le Roy, Frank, additional, Nezam, Dorian, additional, Pruteanu, Diana, additional, Grange, Steven, additional, De Nattes, Tristan, additional, Lemée, Véronique, additional, Guerrot, Dominique, additional, and Candon, Sophie, additional

Published
2024
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5. Intrafamilial Exposure to SARS-CoV-2 Associated with Cellular Immune Response without Seroconversion, France

Author

Gallais, Floriane, Velay, Aurelie, Nazon, Charlotte, Wendling, Marie-Josee, Partisani, Marialuisa, Sibilia, Jean, Candon, Sophie, and Fafi-Kremer, Samira

Subjects
Testing, Observations, Physiological aspects, Host-virus relationships, Disease transmission -- Observations, Epidemics -- Physiological aspects -- France, Immune response -- Testing, COVID-19 -- Physiological aspects
Abstract

Coronavirus disease (COVID-19), caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a pandemic that raises a major concern all around the world (1). To contain the [...]

Published
2021
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10. Does 18F-FDG PET/CT add value to conventional imaging in clinical assessment of chronic disseminated candidiasis?

Author

Rammaert, Blandine, primary, Maunoury, Christophe, additional, Rabeony, Tioka, additional, Correas, Jean-Michel, additional, Elie, Caroline, additional, Alfandari, Serge, additional, Berger, Pierre, additional, Rubio, Marie-Thérèse, additional, Braun, Thorsten, additional, Bakouboula, Prissile, additional, Candon, Sophie, additional, Montravers, Françoise, additional, and Lortholary, Olivier, additional

Published
2022
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11. Combination of lipid metabolism alterations and their sensitivity to inflammatory cytokines in human lipin-1-deficient myoblasts

Author

Michot, Caroline, Mamoune, Asmaa, Vamecq, Joseph, Viou, Mai Thao, Hsieh, Lu-Sheng, Testet, Eric, Lainé, Jeanne, Hubert, Laurence, Dessein, Anne-Frédérique, Fontaine, Monique, Ottolenghi, Chris, Fouillen, Laetitia, Nadra, Karim, Blanc, Etienne, Bastin, Jean, Candon, Sophie, Pende, Mario, Munnich, Arnold, Smahi, Asma, Djouadi, Fatima, Carman, George M., Romero, Norma, de Keyzer, Yves, and de Lonlay, Pascale

Published
2013
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15. Rationale and efficacy of interleukin-1 targeting in Erdheim–Chester disease

Author

Aouba, Achille, Georgin-Lavialle, Sophie, Pagnoux, Christian, Martin Silva, Nicolas, Renand, Amédée, Galateau-Salle, Françoise, Le Toquin, Sophie, Bensadoun, Henri, Larousserie, Frederique, Silvera, Stéphane, Provost, Nicole, Candon, Sophie, Seror, Raphaèle, de Menthon, Mathilde, Hermine, Olivier, Guillevin, Loïc, and Bienvenu, Boris

Published
2010
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20. Dissociated humoral and cellular immune responses after a three-dose schema of BNT162b2 vaccine in patients receiving anti-CD20 monoclonal antibody maintenance treatment for B-cell lymphomas

Author

Candon, Sophie, primary, Lemee, Veronique, additional, Leveque, Emilie, additional, Etancelin, Pascaline, additional, Paquin, Cedric, additional, Carette, Marion, additional, Contentin, Nathalie, additional, Bobee, Victor, additional, Alani, Mustafa, additional, Cardinael, Nathalie, additional, Lepretre, Stephane, additional, Camus, Vincent, additional, Bouclet, Florian, additional, Boulet, Edwige, additional, Menard, Anne-Lise, additional, Lanic, Helene, additional, Stamatoullas, Aspasia, additional, Lemasle, Emilie, additional, Pepin, Louis-Ferdinand, additional, Richard, Doriane, additional, Dubois, Sydney, additional, Tilly, Herve, additional, Dalleac, Alain, additional, Plantier, Jean-Christophe, additional, Etienne, Manuel, additional, and Jardin, Fabrice, additional

Published
2021
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21. Antibody and T Cell Response to SARS-CoV-2 Messenger RNA BNT162b2 Vaccine in Kidney Transplant Recipients and Hemodialysis Patients

Author

Bertrand, Dominique, primary, Hamzaoui, Mouad, additional, Lemée, Veronique, additional, Lamulle, Julie, additional, Hanoy, Mélanie, additional, Laurent, Charlotte, additional, Lebourg, Ludivine, additional, Etienne, Isabelle, additional, Lemoine, Mathilde, additional, Le Roy, Frank, additional, Nezam, Dorian, additional, Plantier, Jean-Christophe, additional, Boyer, Olivier, additional, Guerrot, Dominique, additional, and Candon, Sophie, additional

Published
2021
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22. Evaluation of Humoral Immunity to SARS-CoV-2: Diagnostic Value of a New Multiplex Addressable Laser Bead Immunoassay

Author

Drouot, Laurent, Hantz, Sébastien, Jouen, Fabienne, Velay, Aurélie, Lamia, Bouchra, Veber, Benoit, Sibilia, Jean, Lotellier, Marlène, Candon, Sophie, Alain, Sophie, Fafi-Kremer, Samira, and Boyer, Olivier

Subjects
multiplex, ALBIA, SARS-CoV-2, Methods, luminex, COVID-19, Microbiology
Abstract

Despite efforts to develop anti–severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibody (Ab) immunoassays, reliable serological methods are still needed. We developed a multiplex addressable laser bead immunoassay (ALBIA) to detect and quantify anti-Spike S1 and nucleocapsid N Abs. Recombinant S1 and N proteins were bound to fluorescent beads (ALBIA-IgG-S1/N). Abs were revealed using class-specific anti-human Ig Abs. The performances of the test were analyzed on 575 serum samples including 192 from SARS-CoV-2 polymerase chain reaction–confirmed patients, 13 from seasonal coronaviruses, 70 from different inflammatory/autoimmune diseases, and 300 from healthy donors. Anti-S1 IgM were detected by monoplex ALBIA-IgM-S1. Comparison with chemiluminescent assays or enzyme-linked immunosorbent assays was performed using commercial tests. Multiplex ALBIA-IgG-S1/N was effective in detecting and quantifying anti–SARS-CoV-2 IgG Abs. Two weeks after first symptoms, sensitivity and specificity were 97.7 and 98.0% (anti-S1), and 100 and 98.7% (anti-N), respectively. Agreement with commercial tests was good to excellent, with a higher sensitivity of ALBIA. ALBIA-IgG-S1/N was positive in 53% of patients up to day 7, and in 75% between days 7 and 13. For ALBIA-IgM-S1, sensitivity and specificity were 74.4 and 98.7%, respectively. Patients in intensive care units had higher IgG Ab levels (Mann–Whitney test, p < 0.05). ALBIA provides a robust method for exploring humoral immunity to SARS-CoV-2. Serology should be performed after 2 weeks following first symptoms, when all COVID-19 (coronavirus disease 2019) patients had at least one anti-S1 or anti-N IgG Ab, illustrating the interest of a multiplex test.

Published
2020

23. Antibody response to SARS-CoV-2 mRNA BNT162b2 vaccine in kidney transplant recipients and in-centre and satellite centre haemodialysis patients

Author

Bertrand, Dominique, primary, Hanoy, Mélanie, additional, Edet, Stéphane, additional, Lemée, Veronique, additional, Hamzaoui, Mouad, additional, Laurent, Charlotte, additional, Ludivine, Lebourg, additional, Etienne, Isabelle, additional, Lemoine, Mathilde, additional, Nezam, Dorian, additional, Candon, Sophie, additional, Plantier, Jean-Christophe, additional, Le Roy, Frank, additional, and Guerrot, Dominique, additional

Published
2021
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27. Autoantibodies against granulocyte macrophage colony‐stimulating factor and Nocardia infection in solid organ transplant recipients

Author

Lebeaux, David, primary, Coussement, Julien, additional, Chauvet, Cécile, additional, Matignon, Marie, additional, Scemla, Anne, additional, Bouvier, Nicolas, additional, Dantal, Jacques, additional, Vollaard, Albert M., additional, Wunderink, Herman F., additional, Van Wijngaerden, Eric, additional, Naesens, Maarten, additional, Kamar, Nassim, additional, De Greef, Julien, additional, Guillemain, Romain, additional, Borie, Raphael, additional, and Candon, Sophie, additional

Published
2020
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31. Autoantibodies against granulocyte macrophage colony-stimulating factor and Nocardia infection in solid organ transplant recipients.

Author

UCL - SSS/IREC/SLUC - Pôle St.-Luc, UCL - (SLuc) Service de médecine interne générale, Lebeaux, David, Coussement, Julien, Chauvet, Cécile, Matignon, Marie, Scemla, Anne, Bouvier, Nicolas, Dantal, Jacques, Vollaard, Albert M, Wunderink, Herman F, Van Wijngaerden, Eric, Naesens, Maarten, Kamar, Nassim, De Greef, Julien, Guillemain, Romain, Borie, Raphael, Candon, Sophie, UCL - SSS/IREC/SLUC - Pôle St.-Luc, UCL - (SLuc) Service de médecine interne générale, Lebeaux, David, Coussement, Julien, Chauvet, Cécile, Matignon, Marie, Scemla, Anne, Bouvier, Nicolas, Dantal, Jacques, Vollaard, Albert M, Wunderink, Herman F, Van Wijngaerden, Eric, Naesens, Maarten, Kamar, Nassim, De Greef, Julien, Guillemain, Romain, Borie, Raphael, and Candon, Sophie

Abstract

Dear Editors, Nocardiosis is a rare but potentially severe bacterial opportunistic infection that may occur after solid organ transplantation (SOT), typically among thoracic transplant recipients and/or in recipients with a high degree of immunosuppression due to anti-rejection therapy [1]. However, nocardiosis may also occur late after transplantation among minimally immunosuppressed patients, suggesting that additional risk factors exist [1]. Recently, autoantibodies against granulocyte macrophage colony-stimulating factor (GM-CSF) have been identified among five previously healthy patients with disseminated nocardiosis [2]. These autoantibodies likely promote nocardiosis by reducing neutrophil and macrophage activation, phagocytosis, and bactericidal activity [2]. We hypothesized that anti-GM-CSF autoantibodies might be involved in post-SOT nocardiosis, especially in patients who apparently have a relatively low degree of immunosuppression. [...]

Published
2020

32. Autoantibodies against granulocyte macrophage colony-stimulating factor and Nocardia infection in solid organ transplant recipients

Author

Lebeaux, David, Coussement, Julien, Chauvet, Cécile, Matignon, Marie, Scemla, Anne, Bouvier, Nicolas, Dantal, Jacques, Vollaard, Albert A.M., Wunderink, Herman H.F., Van Wijngaerden, Eric, Naesens, Maarten, Kamar, Nassim, De Greef, Julien, Guillemain, Romain, Borie, Raphael, Candon, Sophie, Lebeaux, David, Coussement, Julien, Chauvet, Cécile, Matignon, Marie, Scemla, Anne, Bouvier, Nicolas, Dantal, Jacques, Vollaard, Albert A.M., Wunderink, Herman H.F., Van Wijngaerden, Eric, Naesens, Maarten, Kamar, Nassim, De Greef, Julien, Guillemain, Romain, Borie, Raphael, and Candon, Sophie

Abstract

SCOPUS: le.j, DecretOANoAutActif, info:eu-repo/semantics/published

Published
2020

34. Humoral response to a fourth dose of mRNA vaccine in kidney transplant recipient responders to three doses of mRNA vaccine.

Author

Nattes, Tristan de, Candon, Sophie, Lemée, Véronique, Laurent, Charlotte, Guerrot, Dominique, and Bertrand, Dominique

Subjects
*HUMORAL immunity, *SARS-CoV-2, *KIDNEY transplantation
Abstract

Kidney transplant recipients (KTRs) experience a low rate of seroconversion after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) messenger RNA (mRNA) vaccine, even after three or even four or five consecutive doses [[1]]. Humoral response was assessed by anti-spike receptor-binding domain IgG antibodies from the ARCHITECT IgG II Quant test (Abbott, Abbott Park, IL, USA). Waning antibody response and cellular immunity 6 months after third dose SARS-Cov-2 mRNA BNT162b2 vaccine in kidney transplant recipients. [Extracted from the article]

Published
2022
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35. CD86 occupancy in belatacept‐treated kidney transplant patients is not associated with clinical and infectious outcomes

Author

Nattes, Tristan, Lebourg, Ludivine, Etienne, Isabelle, Laurent, Charlotte, Lemoine, Mathilde, Dumont, Audrey, Guerrot, Dominique, Jacquot, Serge, Candon, Sophie, and Bertrand, Dominique

Abstract

The CD86 occupancy assay has been developed to measure the number of CD86 molecules unbound to belatacept, but its association with clinical outcomes has not been assessed yet. All kidney transplant patients switched to belatacept in our center between 2016 and 2018 were included. Blood samples were collected before each infusion for 1 year to assess CD86 occupancy by CD86 antibody cytometry staining on the surface of CD14+monocytes. Results were expressed as the median fluorescence intensity (MFI) value of CD86 staining. At each infusion, the MFIDay of infusion/MFIDay 0ratio was calculated. Forty‐one patients were consecutively included. After every 2‐week infusion period, CD86 MFI ratio dropped from 1.00 to 0.73 [0.57–0.98], p = .07. However, this ratio progressively increased to 0.78 [0.53–1.13] at 1 year, which was not statistically different from pre‐switch ratio, p = .4. Over the first year, the MFI ratio coefficient of variation was 31.58% [23.75–38.31]. MFI ratio was not different between patients with or without opportunistic infections: 0.73 [0.60–0.88] versus 0.80 [0.71–1.00], p = .2, or between patients with or without EBV DNAemia, p = .2. Despite previous in vitro results, the CD86 occupancy assay suffers from a high intra‐individual variability and does not appear to be relevant to clinical outcomes. The CD86 receptor occupancy assay is not associated with clinical outcomes in kidney transplant patients treated by belatacept.

Published
2022
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37. Antibiotics in Early Life Alter the Gut Microbiome and Increase Disease Incidence in a Spontaneous Mouse Model of Autoimmune Insulin-Dependent Diabetes

Author

Candon, Sophie, Perez-Arroyo, Alicia, Marquet, Cindy, Valette, Fabrice, Foray, Anne-Perrine, Pelletier, Benjamin, Milani, Christian, Ventura, Marco, Bach, Jean-François, and Chatenoud, Lucienne

Subjects
Male, Mucous Membrane, Incidence, lcsh:R, Correction, lcsh:Medicine, Anti-Bacterial Agents, Gastrointestinal Microbiome, Diabetes Mellitus, Type 1, Mice, Inbred NOD, Vancomycin, Animals, Female, lcsh:Q, Lymphocytes, lcsh:Science, Spleen
Abstract

Insulin-dependent or type 1 diabetes is a prototypic autoimmune disease whose incidence steadily increased over the past decades in industrialized countries. Recent evidence suggests the importance of the gut microbiota to explain this trend. Here, non-obese diabetic (NOD) mice that spontaneously develop autoimmune type 1 diabetes were treated with different antibiotics to explore the influence of a targeted intestinal dysbiosis in the progression of the disease. A mixture of wide spectrum antibiotics (i.e. streptomycin, colistin and ampicillin) or vancomycin alone were administered orally from the moment of conception, treating breeding pairs, and during the postnatal and adult life until the end of follow-up at 40 weeks. Diabetes incidence significantly and similarly increased in male mice following treatment with these two antibiotic regimens. In NOD females a slight yet not significant trend towards an increase in disease incidence was observed. Changes in gut microbiota composition were assessed by sequencing the V3 region of bacterial 16S rRNA genes. Administration of the antibiotic mixture resulted in near complete ablation of the gut microbiota. Vancomycin treatment led to increased Escherichia, Lactobacillus and Sutterella genera and decreased members of the Clostridiales order and Lachnospiraceae, Prevotellaceae and Rikenellaceae families, as compared to control mice. Massive elimination of IL-17-producing cells, both CD4+TCRαβ+ and TCRγδ+ T cells was observed in the lamina propria of the ileum and the colon of vancomycin-treated mice. These results show that a directed even partial ablation of the gut microbiota, as induced by vancomycin, significantly increases type 1 diabetes incidence in male NOD mice thus prompting for caution in the use of antibiotics in pregnant women and newborns.

Published
2016

38. Type I interferon-mediated autoinflammation due to DNase II deficiency

Author

Rodero, Mathieu P., primary, Tesser, Alessandra, additional, Bartok, Eva, additional, Rice, Gillian I., additional, Della Mina, Erika, additional, Depp, Marine, additional, Beitz, Benoit, additional, Bondet, Vincent, additional, Cagnard, Nicolas, additional, Duffy, Darragh, additional, Dussiot, Michael, additional, Frémond, Marie-Louise, additional, Gattorno, Marco, additional, Guillem, Flavia, additional, Kitabayashi, Naoki, additional, Porcheray, Fabrice, additional, Rieux-Laucat, Frederic, additional, Seabra, Luis, additional, Uggenti, Carolina, additional, Volpi, Stefano, additional, Zeef, Leo A H., additional, Alyanakian, Marie-Alexandra, additional, Beltrand, Jacques, additional, Bianco, Anna Monica, additional, Boddaert, Nathalie, additional, Brouzes, Chantal, additional, Candon, Sophie, additional, Caorsi, Roberta, additional, Charbit, Marina, additional, Fabre, Monique, additional, Faletra, Flavio, additional, Girard, Muriel, additional, Harroche, Annie, additional, Hartmann, Evelyn, additional, Lasne, Dominique, additional, Marcuzzi, Annalisa, additional, Neven, Bénédicte, additional, Nitschke, Patrick, additional, Pascreau, Tiffany, additional, Pastore, Serena, additional, Picard, Capucine, additional, Picco, Paolo, additional, Piscianz, Elisa, additional, Polak, Michel, additional, Quartier, Pierre, additional, Rabant, Marion, additional, Stocco, Gabriele, additional, Taddio, Andrea, additional, Uettwiller, Florence, additional, Valencic, Erica, additional, Vozzi, Diego, additional, Hartmann, Gunther, additional, Barchet, Winfried, additional, Hermine, Olivier, additional, Bader-Meunier, Brigitte, additional, Tommasini, Alberto, additional, and Crow, Yanick J., additional

Published
2017
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39. Antibiotics in Early Life Alter the Gut Microbiome and Increase Disease Incidence in a Spontaneous Mouse Model of Autoimmune Insulin-Dependent Diabetes

Author

Candon, Sophie, Perez-Arroyo, Alicia, Marquet, Cindy, Valette, Fabrice, Foray, Anne-Perrine, Pelletier, Benjamin, Milani, Cristian, Ventura, Marco, Bach, Jean-François, Chatenoud, Lucienne, Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Sorbonne Paris Cité (USPC), Academie des Sciences, Diabète de Type 1 : mécanismes et traitements immunologiques, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Académie des Sciences, and Institut de France

Subjects
[SDV]Life Sciences [q-bio], lcsh:R, lcsh:Medicine, [SDV.IMM]Life Sciences [q-bio]/Immunology, lcsh:Q, lcsh:Science, ComputingMilieux_MISCELLANEOUS, Research Article
Abstract

Insulin-dependent or type 1 diabetes is a prototypic autoimmune disease whose incidence steadily increased over the past decades in industrialized countries. Recent evidence suggests the importance of the gut microbiota to explain this trend. Here, non-obese diabetic (NOD) mice that spontaneously develop autoimmune type 1 diabetes were treated with different antibiotics to explore the influence of a targeted intestinal dysbiosis in the progression of the disease. A mixture of wide spectrum antibiotics (i.e. streptomycin, colistin and ampicillin) or vancomycin alone were administered orally from the moment of conception, treating breeding pairs, and during the postnatal and adult life until the end of follow-up at 40 weeks. Diabetes incidence significantly and similarly increased in male mice following treatment with these two antibiotic regimens. In NOD females a slight yet not significant trend towards an increase in disease incidence was observed. Changes in gut microbiota composition were assessed by sequencing the V3 region of bacterial 16S rRNA genes. Administration of the antibiotic mixture resulted in near complete ablation of the gut microbiota. Vancomycin treatment led to increased Escherichia, Lactobacillus and Sutterella genera and decreased members of the Clostridiales order and Lachnospiraceae, Prevotellaceae and Rikenellaceae families, as compared to control mice. Massive elimination of IL-17-producing cells, both CD4+TCRαβ+ and TCRγδ+ T cells was observed in the lamina propria of the ileum and the colon of vancomycin-treated mice. These results show that a directed even partial ablation of the gut microbiota, as induced by vancomycin, significantly increases type 1 diabetes incidence in male NOD mice thus prompting for caution in the use of antibiotics in pregnant women and newborns.

Published
2015
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40. Correction: Antibiotics in Early Life Alter the Gut Microbiome and Increase Disease Incidence in a Spontaneous Mouse Model of Autoimmune Insulin-Dependent Diabetes

Author

Candon, Sophie, primary, Perez-Arroyo, Alicia, additional, Marquet, Cindy, additional, Valette, Fabrice, additional, Foray, Anne-Perrine, additional, Pelletier, Benjamin, additional, Milani, Christian, additional, Ventura, Marco, additional, Bach, Jean-François, additional, and Chatenoud, Lucienne, additional

Published
2016
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41. Long-term CD4 lymphopenia is associated with accelerated decline of kidney allograft function

Author

Luque, Yosu, primary, Jamme, Matthieu, additional, Rabant, Marion, additional, DeWolf, Susan, additional, Noël, Laure-Hélène, additional, Thervet, Eric, additional, Chatenoud, Lucienne, additional, Snanoudj, Renaud, additional, Anglicheau, Dany, additional, Legendre, Christophe, additional, Candon, Sophie, additional, and Zuber, Julien, additional

Published
2015
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42. Four-year metabolic outcome of a randomised controlled CD3-antibody trial in recent-onset type 1 diabetic patients depends on their age and baseline residual beta cell mass.

Author

Keymeulen, B, Walter, M, Mathieu, C, Kaufman, L., Gorus, F, Hilbrands, Robert, Vandemeulebroucke, Evy, Van de Velde, U, Crenier, Laurent, De Block, Christophe, Candon, Sophie, Waldmann, Herman, Ziegler, A G, Chatenoud, Lucienne, Pipeleers, D, Keymeulen, B, Walter, M, Mathieu, C, Kaufman, L., Gorus, F, Hilbrands, Robert, Vandemeulebroucke, Evy, Van de Velde, U, Crenier, Laurent, De Block, Christophe, Candon, Sophie, Waldmann, Herman, Ziegler, A G, Chatenoud, Lucienne, and Pipeleers, D

Abstract

The aim of the study was to examine the 48 month outcome of treating recent-onset type 1 diabetic patients for 6 days with humanised CD3-antibody, ChAglyCD3., Clinical Trial, Phase II, Journal Article, Multicenter Study, Randomized Controlled Trial, Research Support, Non-U.S. Gov't, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2010

43. Insulin needs after CD3-antibody therapy in new-onset type 1 diabetes.

Author

Keymeulen, Bart, Vandemeulebroucke, Evy, Ziegler, Anette G, Mathieu, Chantal, Kaufman, Leonard, Hale, Geoff, Gorus, Frans, Goldman, Michel, Walter, Markus, Candon, Sophie, Schandené, Liliane, Crenier, Laurent, De Block, Christophe, Seigneurin, Jean-Marie, De Pauw, Pieter, Pierard, Denis, Weets, Ilse, Rebello, Peppy, Bird, Pru, Berrie, Eleanor, Frewin, Mark, Waldmann, Herman, Bach, Jean-François, Pipeleers, Daniel, Chatenoud, Lucienne, Keymeulen, Bart, Vandemeulebroucke, Evy, Ziegler, Anette G, Mathieu, Chantal, Kaufman, Leonard, Hale, Geoff, Gorus, Frans, Goldman, Michel, Walter, Markus, Candon, Sophie, Schandené, Liliane, Crenier, Laurent, De Block, Christophe, Seigneurin, Jean-Marie, De Pauw, Pieter, Pierard, Denis, Weets, Ilse, Rebello, Peppy, Bird, Pru, Berrie, Eleanor, Frewin, Mark, Waldmann, Herman, Bach, Jean-François, Pipeleers, Daniel, and Chatenoud, Lucienne

Abstract

BACKGROUND: Type 1 diabetes mellitus is a T-cell-mediated autoimmune disease that leads to a major loss of insulin-secreting beta cells. The further decline of beta-cell function after clinical onset might be prevented by treatment with CD3 monoclonal antibodies, as suggested by the results of a phase 1 study. To provide proof of this therapeutic principle at the metabolic level, we initiated a phase 2 placebo-controlled trial with a humanized antibody, an aglycosylated human IgG1 antibody directed against CD3 (ChAglyCD3). METHODS: In a multicenter study, 80 patients with new-onset type 1 diabetes were randomly assigned to receive placebo or ChAglyCD3 for six consecutive days. Patients were followed for 18 months, during which their daily insulin needs and residual beta-cell function were assessed according to glucose-clamp-induced C-peptide release before and after the administration of glucagon. RESULTS: At 6, 12, and 18 months, residual beta-cell function was better maintained with ChAglyCD3 than with placebo. The insulin dose increased in the placebo group but not in the ChAglyCD3 group. This effect of ChAglyCD3 was most pronounced among patients with initial residual beta-cell function at or above the 50th percentile of the 80 patients. In this subgroup, the mean insulin dose at 18 months was 0.22 IU per kilogram of body weight per day with ChAglyCD3, as compared with 0.61 IU per kilogram with placebo (P<0.001). In this subgroup, 12 of 16 patients who received ChAglyCD3 (75 percent) received minimal doses of insulin (< or =0.25 IU per kilogram per day) as compared with none of the 21 patients who received placebo. Administration of ChAglyCD3 was associated with a moderate "flu-like" syndrome and transient symptoms of Epstein-Barr viral mononucleosis. CONCLUSIONS: Short-term treatment with CD3 antibody preserves residual beta-cell function for at least 18 months in patients with recent-onset type 1 diabetes., Clinical Trial, Clinical Trial, Phase II, Journal Article, Multicenter Study, Randomized Controlled Trial, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2005

45. Rituximab in Severe Lupus Nephritis: Early B-Cell Depletion Affects Long-Term Renal Outcome

Author

Melander, Catherine, primary, Sallée, Marion, additional, Trolliet, Pierre, additional, Candon, Sophie, additional, Belenfant, Xavier, additional, Daugas, Eric, additional, Rémy, Phillipe, additional, Zarrouk, Virginie, additional, Pillebout, Evangéline, additional, Jacquot, Christian, additional, Boffa, Jean-Jacques, additional, Karras, Alexandre, additional, Masse, Virginie, additional, Lesavre, Philippe, additional, Elie, Caroline, additional, Brocheriou, Isabelle, additional, Knebelmann, Bertrand, additional, Noël, Laure-Hélène, additional, and Fakhouri, Fadi, additional

Published
2009
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46. Long-term CD4 lymphopenia is associated with accelerated decline of kidney allograft function.

Author

Yosu Luque, Jamme, Matthieu, Rabant, Marion, DeWolf, Susan, Noël, Laure-Hélène, Thervet, Eric, Chatenoud, Lucienne, Snanoudj, Renaud, Anglicheau, Dany, Legendre, Christophe, Candon, Sophie, and Zuber, Julien

Subjects
LYMPHOPENIA, LEUCOPENIA, HOMOGRAFTS, T cells, IMMUNOLOGICAL deficiency syndromes
Abstract

Background. Persistent CD4 T-cell lymphopenia after kidney transplantation has been associated with an increased occurrence of opportunistic infections, malignancies and even mortality, but studies have focussed only on the first few years after kidney transplantation. In this study, we investigated the risk factors and clinical significance of long-term profound CD4 lymphopenia detected ≥10 years after renal transplantation. Methods. Between 2007 and 2010, 6206 CD4 T-cell counts, including 1507 counts <300/mm3, were identified in an active cohort of 1876 kidney transplant patients. We identified 27 HIV-negative lymphopenic kidney transplant recipients out of 513 patients with graft survival over 10 years. We compared this cohort to 54 non-lymphopenic controls matched for the date of kidney transplantation. Results. The prevalence of CD4 lymphopenia 10 years after transplantation was 5.3%. CD4 T-cell lymphopenia was associated with significantly lower thymic output and with B-cell lymphopenia (P < 0.05). The duration of pre-transplant dialysis, but not the use of lymphopenic induction or recipient age, was significantly associated with a persistent CD4 lymphopenia (6.1 versus 3.0 years, P = 0.008). CD4 lymphopenia was associated with a higher frequency of cancer (50 versus 29.6%, P = 0.047). Most strikingly, long-term lymphopenia was significantly and independently associated with an accelerated decline in renal allograft function (P = 0.005), despite a similar rate of biopsy-proven acute rejection and comparable immunosuppression. Conclusions. Our study shows an association between longterm CD4 T-cell lymphopenia in kidney recipients and malignancy and an accelerated decline of kidney allograft function. [ABSTRACT FROM AUTHOR]

Published
2016
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47. Specific overexpression of rheumatoid arthritis–associated HLA–DR alleles and presentation of low-affinity peptides

Author

Kerlan-Candon, Sophie, Louis-Plence, Pascale, Wiedemann, Agnes, Combe, Bernard, Clot, Jacques, Eliaou, Jean-François, and Pinet, Valérie

Abstract

To compare levels of HLA–DR expression in rheumatoid arthritis (RA) patients and healthy controls for whom an ordered expression according to the DR alleles is demonstrated and to test the functional consequences of this expression on peptide presentation. Using monoclonal antibodies that recognize different DRB1 alleles, DR molecules were quantitated at the surface of the peripheral blood B cells of 23 RA patients and 17 healthy subjects. The functional consequences of the level of DR surface expression was tested using a universal model of antigen presentation and mutated peptides with variable affinities for the T cell receptor. In healthy subjects, surface HLA–DR molecules were expressed at different levels according to allele (DR53, DR4, and DR11 less than DR1 less than DR7 less than DR15). In RA patients, this hierarchy was not conserved and, furthermore, the density of RA-associated DR4 and DR1 molecules was enhanced in patients compared with the basal density in healthy individuals. We demonstrated that an increased expression of DR molecules at the surface of antigen-presenting cells allowed a noteworthy presentation of low-affinity peptides that under normal conditions are not efficient in generating a T cell response at physiologic surface density of the DR molecules. Our results suggest that the specific overexpression of RA-associated HLA molecules could be responsible for the presentation of low-affinity autopeptides and therefore the activation of peripheral autoreactive T cells.

Published
2001
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49. Type I interferon-mediated autoinflammation due to DNase II deficiency

Author

Flavio Faletra, Gabriele Stocco, Evelyn Hartmann, Chantal Brouzes, Flavia Guillem, Fabrice Porcheray, Florence Uettwiller, Carolina Uggenti, Diego Vozzi, Marion Rabant, Capucine Picard, Nicolas Cagnard, Elisa Piscianz, Olivier Hermine, Andrea Taddio, Sophie Candon, Gunther Hartmann, Leo A. H. Zeef, Pierre Quartier, Marie Alexandra Alyanakian, Brigitte Bader-Meunier, Benoit Beitz, Gillian I. Rice, Muriel Girard, Monique Fabre, Alberto Tommasini, Dominique Lasne, Marine Depp, Nathalie Boddaert, Mathieu P Rodero, Stefano Volpi, Marco Gattorno, Yanick J. Crow, Eva Bartok, Michael Dussiot, Michel Polak, Tiffany Pascreau, Roberta Caorsi, Erika Della Mina, Naoki Kitabayashi, Annalisa Marcuzzi, Vincent Bondet, Paolo Picco, Luis Seabra, Jacques Beltrand, Erica Valencic, Marie-Louise Frémond, Bénédicte Neven, Frédéric Rieux-Laucat, Darragh Duffy, Alessandra Tesser, Patrick Nitschke, Anna Monica Bianco, Marina Charbit, Annie Harroche, Serena Pastore, Winfried Barchet, Laboratory of neurogenetics and neuroinflammation (Equipe Inserm U1163), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Trieste, University of Bonn, Academic Unit of Medical Genetic, University of Manchester [Manchester], Microbiology Technology Institute, BIOASTER Microbiology Technology Institute [Lyon], Immunobiologie des Cellules dendritiques, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Structure Fédérative de Recherche Necker (SFR Necker - UMS 3633 / US24), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Giannina Gaslini Institute, Istituto Giannina Gaslini, Genova, Immunologia Clinica e Sperimentale, Service d'immuno-hématologie pédiatrique [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service de Radiologie et imagerie médicale [CHU Necker], Laboratory of molecular mechanisms of hematologic disorders and therapeutic implications (ERL 8254 - Equipe Inserm U1163), Service de néphrologie pédiatrique [CHU Necker], Hôpital Bicêtre, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, Plate Forme Paris Descartes de Bioinformatique (BIP-D), Université Paris Descartes - Paris 5 (UPD5), Centre d'étude des Déficits Immunitaires, Service d'endocrinologie, gynécologie et diabétologie pédiatriques [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Department of Life Sciences, Institute of Clinical Chemistry and Pharmacology, Center for Integrated Oncology, University Hospital of Bonn, Service d'Hématologie Adulte, IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy, Y.J.C. acknowledges the European Research Council (GA 309449), and a state subsidymanaged by the National Research Agency (France) under the 'Investments for the Future'program bearing the reference ANR-10-IAHU-01. We thank ImmunoQure AGfor sharing of antibodies used to assess interferon alpha protein levels in the Simoa assay.M.-L.F. is supported by the Institut National de la Santé et de la Recherche Médicale(Grant number 000427993). A.T. and M.G. acknowledge the Italian Telethon (Grant no.GGP15241A). A.T. acknowledges the Institute for Maternal and Child Health-IRCCS'Burlo Garofolo' (RC 17/2014 funded by Italian Ministry of Health, art 12 and 12bis D.lgs 502/92), the 'Associazione Azzurra Malattie Rare'and the 'Beneficientia Stiftung in Vaduz'. We would like to thank Olivier pellet and Jerome Megret from theflow cytometry platform at SFR Necker (INSERM US24-CNRS UMS 3633) for their help withperipheral blood mononuclear cell subset isolation. We would like to thank the Geno-mics Platform, INSERM UMR1163 for whole-exome sequencing. E.B., G.H., and W.B.acknowledge DZIF funding and German Research Foundation (DFG) grants EXC1023:ImmunoSensation, CRCs 670 and 704, ANR-10-IAHU-0001,Imagine,Institut Hospitalo-Universitaire Imagine(2010), European Project: 309449,EC:FP7:ERC,ERC-2012-StG_20111109,T1-IFN(2013), Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques (LCBPT - UMR 8601), Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS), BIOASTER, Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Università degli studi di Trieste = University of Trieste, Universität Bonn = University of Bonn, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University Hospital Bonn, Vougny, Marie-Christine, Instituts Hospitalo-Universitaires - Institut Hospitalo-Universitaire Imagine - - Imagine2010 - ANR-10-IAHU-0001 - IAHU - VALID, Definition and characterization of type I interferonopathies - T1-IFN - - EC:FP7:ERC2013-03-01 - 2018-02-28 - 309449 - VALID, Rodero, Mathieu P., Tesser, Alessandra, Bartok, Eva, Rice, Gillian I., Della Mina, Erika, Depp, Marine, Beitz, Benoit, Bondet, Vincent, Cagnard, Nicola, Duffy, Darragh, Dussiot, Michael, Frã©mond, Marie-Louise, Gattorno, Marco, Guillem, Flavia, Kitabayashi, Naoki, Porcheray, Fabrice, Rieux-Laucat, Frederic, Seabra, Lui, Uggenti, Carolina, Volpi, Stefano, Zeef, Leo A. H., Alyanakian, Marie-Alexandra, Beltrand, Jacque, Bianco, Anna Monica, Boddaert, Nathalie, Brouzes, Chantal, Candon, Sophie, Caorsi, Roberta, Charbit, Marina, Fabre, Monique, Faletra, Flavio, Girard, Muriel, Harroche, Annie, Hartmann, Evelyn, Lasne, Dominique, Marcuzzi, Annalisa, Neven, Bã©nã©dicte, Nitschke, Patrick, Pascreau, Tiffany, Pastore, Serena, Picard, Capucine, Picco, Paolo, Piscianz, Elisa, Polak, Michel, Quartier, Pierre, Rabant, Marion, Stocco, Gabriele, Taddio, Andrea, Uettwiller, Florence, Valencic, Erica, Vozzi, Diego, Hartmann, Gunther, Barchet, Winfried, Hermine, Olivier, Bader-Meunier, Brigitte, Tommasini, Alberto, and Crow, Yanick J.

Subjects
Genetics and Molecular Biology (all), Male, 0301 basic medicine, Erythroblasts, [SDV]Life Sciences [q-bio], DNASE2, type I interferon, autoinflammation, exome sequencing, Up-Regulation/drug effects, General Physics and Astronomy, Erythroblasts/immunology, DNASE2, type I interferon, autoinflammation, exome sequencing, Biochemistry, LS3_11, 0302 clinical medicine, Interferon, Interferon-alpha/blood, Membranoproliferative glomerulonephritis, STAT1, Phosphorylation, lcsh:Science, Child, ComputingMilieux_MISCELLANEOUS, Deoxyribonucleases, Multidisciplinary, biology, RNA, Messenger/analysis, Chemistry (all), Endodeoxyribonucleases/deficiency, Up-Regulation, 3. Good health, STAT1 Transcription Factor, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, STAT1 Transcription Factor/metabolism, Antibody, Signal Transduction, medicine.drug, STAT3 Transcription Factor, [SDV.IMM] Life Sciences [q-bio]/Immunology, Adolescent, Science, Alpha interferon, Antiviral Agents/pharmacology, Hematopoiesis/immunology, Antiviral Agents, Article, General Biochemistry, Genetics and Molecular Biology, Deoxyribonucleases/deficiency, NO, Physics and Astronomy (all), 03 medical and health sciences, Downregulation and upregulation, medicine, Humans, RNA, Messenger, Signal Transduction/immunology, Endodeoxyribonucleases, Innate immune system, Sequence Analysis, RNA, Gene Expression Profiling, Hereditary Autoinflammatory Diseases, Interferon-alpha, General Chemistry, medicine.disease, Hematopoiesis, 030104 developmental biology, STAT3 Transcription Factor/metabolism, Hereditary Autoinflammatory Diseases/blood, Mutation, Immunology, biology.protein, Nucleic acid, lcsh:Q, Biochemistry, Genetics and Molecular Biology (all), 030215 immunology
Abstract

Microbial nucleic acid recognition serves as the major stimulus to an antiviral response, implying a requirement to limit the misrepresentation of self nucleic acids as non-self and the induction of autoinflammation. By systematic screening using a panel of interferon-stimulated genes we identify two siblings and a singleton variably demonstrating severe neonatal anemia, membranoproliferative glomerulonephritis, liver fibrosis, deforming arthropathy and increased anti-DNA antibodies. In both families we identify biallelic mutations in DNASE2, associated with a loss of DNase II endonuclease activity. We record increased interferon alpha protein levels using digital ELISA, enhanced interferon signaling by RNA-Seq analysis and constitutive upregulation of phosphorylated STAT1 and STAT3 in patient lymphocytes and monocytes. A hematological disease transcriptomic signature and increased numbers of erythroblasts are recorded in patient peripheral blood, suggesting that interferon might have a particular effect on hematopoiesis. These data define a type I interferonopathy due to DNase II deficiency in humans., Nucleic acid sensing is important to ensure that an innate immune response is only mounted against microbial nucleic acid. Here, the authors identify loss-of-function mutations in the DNASE2 gene that cause type I interferon-mediated autoinflammation due to enhanced systemic interferon signaling.

Published
2017
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50. Does 18 F-FDG PET/CT add value to conventional imaging in clinical assessment of chronic disseminated candidiasis?

Author

Rammaert B, Maunoury C, Rabeony T, Correas JM, Elie C, Alfandari S, Berger P, Rubio MT, Braun T, Bakouboula P, Candon S, Montravers F, and Lortholary O

Abstract

Background: Chronic disseminated candidiasis (CDC) classically occurs after profound and prolonged neutropenia. The aim of the CANHPARI study was to assess the clinical value of adding 18 F-fluorodeoxyglucose PET/CT to conventional radiology for initial and subsequent evaluations of CDC., Materials and Methods: A pilot prospective study was conducted in 23 French onco-hematological centers from 2013 to 2017 (NCT01916057). Patients ≥ 18 y.o. suspected for CDC on abdominal conventional imaging (CT or MRI) were included. PET/CT and conventional imaging were performed at baseline and month 3 (M3). Follow-up was assessed until M12. The primary outcome measure was the global response at M3, i.e., apyrexia and complete response to PET/CT. The secondary outcome measure consists in comparison between responses to PET/CT and conventional imaging at diagnosis and M3., Results: Among 52 included patients, 44 were evaluable (20 probable and 24 possible CDC); 86% had acute leukemia, 55% were male (median age 47 years). At diagnosis, 34% had fever and conventional imaging was always abnormal with microabscesses on liver and spleen in 66%, liver in 25%, spleen in 9%. Baseline PET/CT showed metabolic uptake on liver and/or spleen in 84% but did not match with lesion localizations on conventional imaging in 32%. M3 PET/CT showed no metabolic uptake in 13 (34%) patients, 11 still having pathological conventional imaging. Global response at M3 was observed in eight patients., Conclusion: Baseline PET/CT does not replace conventional imaging for initial staging of CDC lesions but should be performed after 3 months of antifungal therapy., Clinical Trial Registration: [www.clinicaltrials.gov], identifier [NCT01916057]., Competing Interests: BR has travel grants from Pfizer and MSD, speaker’s fees from MSD, Gilead, Astellas, and Iqone. SA has travel grants from MSD and Gilead, and speaker’s fee from Gilead. PiB has travel grants from Astellas, Pfizer, MSD, and Gilead, and speaker’s fee from MSD. OL speaker’s fees from MSD, Gilead, Astellas, Pfizer, and F2G, consultant Gilead. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Rammaert, Maunoury, Rabeony, Correas, Elie, Alfandari, Berger, Rubio, Braun, Bakouboula, Candon, Montravers and Lortholary.)

Published
2022
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