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19 results on '"Bismuth, Jacky"'

1. Estrogen-mediated downregulation of AIRE influences sexual dimorphism in autoimmune diseases

Author

Dragin, Nadine, Bismuth, Jacky, Cizeron-Clairac, Geraldine, Biferi, Maria Grazia, Berthault, Claire, Serraf, Alain, Nottin, Remi, Klatzmann, David, Cumano, Ana, Barkats, Martine, Panse, Rozen Le, and Berrih-Aknin, Sonia

Subjects
Genetic regulation -- Health aspects, Estrogen -- Health aspects, Transcription factors -- Properties, Autoimmune diseases -- Genetic aspects -- Development and progression, Health care industry
Abstract

Autoimmune diseases affect 5% to 8% of the population, and females are more susceptible to these diseases than males. Here, we analyzed human thymic transcriptome and revealed sex-associated differences in the expression of tissue-specific antigens that are controlled by the autoimmune regulator (AIRE), a key factor in central tolerance. We hypothesized that the level of AIRE is linked to sexual dimorphism susceptibility to autoimmune diseases. In human and mouse thymus, females expressed less AIRE (mRNA and protein) than males after puberty. These results were confirmed in purified murine thymic epithelial cells (TECs). We also demonstrated that AIRE expression is related to sexual hormones, as male castration decreased AIRE thymic expression and estrogen receptor a-deficient mice did not show a sex disparity for AIRE expression. Moreover, estrogen treatment resulted in downregulation of AIRE expression in cultured human TECs, human thymic tissue grafted to immunodeficient mice, and murine fetal thymus organ cultures. AIRE levels in human thymus grafted in immunodeficient mice depended upon the sex of the recipient. Estrogen also upregulated the number of methylated CpG sites in the AIRE promoter. Together, our results indicate that in females, estrogen induces epigenetic changes in the AIRE gene, leading to reduced AIRE expression under a threshold that increases female susceptibility to autoimmune diseases., Introduction Autoimmune diseases, a group of 70 different diseases, represent the fifth leading cause of death by disease among females of reproductive age (1, 2). As suggested by several studies, [...]

Published
2016
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10. Preconditioned mesenchymal stem cells treat myasthenia gravis in a humanized preclinical model

Author

Sudres, Muriel, primary, Maurer, Marie, additional, Robinet, Marieke, additional, Bismuth, Jacky, additional, Truffault, Frédérique, additional, Girard, Diane, additional, Dragin, Nadine, additional, Attia, Mohamed, additional, Fadel, Elie, additional, Santelmo, Nicola, additional, Sicsic, Camille, additional, Brenner, Talma, additional, and Berrih-Aknin, Sonia, additional

Published
2017
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11. IL-6 and Akt are involved in muscular pathogenesis in myasthenia gravis

Author

Maurer, Marie, primary, Bougoin, Sylvain, additional, Feferman, Tali, additional, Frenkian, Mélinée, additional, Bismuth, Jacky, additional, Mouly, Vincent, additional, Clairac, Geraldine, additional, Tzartos, Socrates, additional, Fadel, Elie, additional, Eymard, Bruno, additional, Fuchs, Sara, additional, Souroujon, Miriam C, additional, and Berrih-Aknin, Sonia, additional

Published
2015
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12. Microarrays Reveal Distinct Gene Signatures in the Thymus of Seropositive and Seronegative Myasthenia Gravis Patients and the Role of CC Chemokine Ligand 21 in Thymic Hyperplasia1

Author

Le Panse, Rozen, Cizeron-Clairac, Géraldine, Bismuth, Jacky, and Berrih-Aknin, Sonia

Subjects
Adult, Male, Chemokine CCL21, Gene Expression Profiling, Gene Expression, Thymus Gland, Article, Chemokines, CC, Myasthenia Gravis, Humans, Female, Thymus Hyperplasia, Autoantibodies, Oligonucleotide Array Sequence Analysis
Abstract

Myasthenia gravis (MG) is an autoimmune disease mainly caused by antiacetylcholine receptor autoantibodies (seropositive (SP) disease) or by Abs against unknown autoantigenic target(s) (seronegative (SN) disease). Thymectomy is usually beneficial although thymic hyperplasia with ectopic germinal centers is mainly observed in SP MG. To understand the role of thymus in the disease process, we compared the thymic transcriptome of non-MG adults to those of SP patients with a low or high degree of hyperplasia or SN patients. Surprisingly, an overexpression of MHC class II, Ig, and B cell marker genes is observed in SP but also SN MG patients. Moreover, we demonstrate an overexpression of CXCL13 in all MG thymuses leading probably to the generalized B cell infiltration. However, we find different chemotactic properties for MG subgroups and, especially, a specific overexpression of CCL21 in hyperplastic thymuses triggering most likely ectopic germinal center development. Besides, SN patients present a peculiar signature with an abnormal expression of genes involved in muscle development and synaptic transmission, but also genes implicated in host response, suggesting that viral infection might be related to SN MG. Altogether, these results underline differential pathogenic mechanisms in the thymus of SP and SN MG and propose new research areas.

Published
2006

19. [Untitled]

Author

Dragin, Nadine, Bismuth, Jacky, Cizeron-Clairac, Géraldine, Biferi, Maria Grazia, Berthault, Claire, Serraf, Alain, Nottin, Rémi, Klatzmann, David, Cumano, Ana, Barkats, Martine, Le Panse, Rozen, Berrih-Aknin, Sonia, Centre de recherche en myologie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Association française contre les myopathies (AFM-Téléthon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Remodelage tissulaire et fonctionnel : signalisation et physio-pathologie (RTFSPP), Centre National de la Recherche Scientifique (CNRS)-Centre chirurgical Marie Lannelongue-Université Paris-Sud - Paris 11 (UP11), Cellule Pasteur, Université Paris Diderot - Paris 7 (UPD7)-PRES Sorbonne Paris Cité, Lymphopoïèse, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Chirurgical Marie Lannelongue (CCML), Centre chirurgical Marie Lannelongue, Immunologie - Immunopathologie - Immunothérapie (I3), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de Myologie, Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Association française contre les myopathies (AFM-Téléthon)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Pierre et Marie Curie - Paris 6 (UPMC), This work was supported by MYASTAID (LSHM-CT-2006-037833) and FIGHT-MG (HEALTH-2009-242-210) grants from the European Community and a grant from the Association Française contre les Myopathies obtained by S. Berrih-Aknin., European Project: 38962,MYASTAID, European Project: 242210,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,FIGHT-MG(2009), Université Paris-Sud - Paris 11 (UP11)-Centre Chirurgical Marie Lannelongue (CCML)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Association française contre les myopathies (AFM-Téléthon)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), HAL UPMC, Gestionnaire, Development of models to improve management of Myasthenia Gravis: From basic knowledge to clinical application - MYASTAID - 38962 - OLD, and Myasthenias, a group of immune mediated neurological diseases: from etiology to therapy. - FIGHT-MG - - EC:FP7:HEALTH2009-12-01 - 2014-05-31 - 242210 - VALID

Subjects
0301 basic medicine, medicine.medical_specialty, medicine.drug_class, Population, Estrogen receptor, Biology, MESH: Estrogens, 03 medical and health sciences, MESH: DNA Methylation, 0302 clinical medicine, MESH: Autoimmune Diseases, MESH: Child, Internal medicine, Male castration, medicine, MESH: Animals, MESH: Mice, Inbred C3H, MESH: CpG Islands, education, MESH: Mice, MESH: Estrogen Receptor alpha, MESH: Adolescent, education.field_of_study, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, MESH: Humans, MESH: Middle Aged, MESH: Child, Preschool, MESH: Adult, MESH: Thymus Gland, MESH: Transcription Factors, General Medicine, Autoimmune regulator, MESH: Gene Expression Regulation, MESH: Infant, MESH: Male, Thymic Tissue, 030104 developmental biology, Endocrinology, Estrogen, Central tolerance, MESH: Female, Estrogen receptor alpha, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, MESH: Sex Characteristics, MESH: Cells, Cultured, 030215 immunology
Abstract

International audience; Autoimmune diseases affect 5% to 8% of the population, and females are more susceptible to these diseases than males. Here, we analyzed human thymic transcriptome and revealed sex-associated differences in the expression of tissue-specific antigens that are controlled by the autoimmune regulator (AIRE), a key factor in central tolerance. We hypothesized that the level of AIRE is linked to sexual dimorphism susceptibility to autoimmune diseases. In human and mouse thymus, females expressed less AIRE (mRNA and protein) than males after puberty. These results were confirmed in purified murine thymic epithelial cells (TECs). We also demonstrated that AIRE expression is related to sexual hormones, as male castration decreased AIRE thymic expression and estrogen receptor α-deficient mice did not show a sex disparity for AIRE expression. Moreover, estrogen treatment resulted in downregulation of AIRE expression in cultured human TECs, human thymic tissue grafted to immunodeficient mice, and murine fetal thymus organ cultures. AIRE levels in human thymus grafted in immunodeficient mice depended upon the sex of the recipient. Estrogen also upregulated the number of methylated CpG sites in the AIRE promoter. Together, our results indicate that in females, estrogen induces epigenetic changes in the AIRE gene, leading to reduced AIRE expression under a threshold that increases female susceptibility to autoimmune diseases.

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