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1. Bromodomain and extraterminal (BET) protein inhibition of IgG/IgE production in murine B cells is counter-balanced by a strong Th2 bias

Author

Bernhard Ryffel, Yolla Makhour, Zeinab Dalloul, Pauline Chenuet, Jean-Claude Aldigier, Michel Cogné, François Boyer, Marie Best, Valérie F. J. Quesniaux, Sandrine Le Noir, Dieudonnée Togbe, Jeanne Cook-Moreau, Mylène Gador, Nicolas Fazilleau, Iman Dalloul, Jonchère, Laurent, Rôle de la classe des Ig / BCR dans les interactions cellulaires supportant la mémoire immune et impact immunopathologique - - Ig-MemImpact2016 - ANR-16-CE15-0019 - AAPG2016 - VALID, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM), Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Artimmune SAS, Lebanese University [Beirut] (LU), Microenvironment, Cell Differentiation, Immunology and Cancer (MICMAC), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), PGA1 RF20180207070, Fondation ARC pour la Recherche sur le Cancer, ANR‐16‐CE15‐0019‐01, Agence Nationale de la Recherche, 2016‐00110366, European Regional Development Fund, ANR-16-CE15-0019,Ig-MemImpact,Rôle de la classe des Ig / BCR dans les interactions cellulaires supportant la mémoire immune et impact immunopathologique(2016), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), and Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)

Subjects
0301 basic medicine, Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, Immunoglobulin E, immune response, Allergic inflammation, 03 medical and health sciences, 0302 clinical medicine, Immune system, [SDV.CAN] Life Sciences [q-bio]/Cancer, medicine, allergic inflammation, Immunology and Allergy, General Nursing, biology, Chemistry, RC581-607, Eosinophil, Bromodomain, 030104 developmental biology, medicine.anatomical_structure, Immunoglobulin class switching, [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, [SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, [SDV.IMM.IA] Life Sciences [q-bio]/Immunology/Adaptive immunology, Humoral immunity, biology.protein, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, Original Article, Immunologic diseases. Allergy, Antibody, bromodomain inhibition, antibody class switching, 030215 immunology
Abstract

Objectives Inhibitors of bromodomain and extra terminal domain (BET) proteins are a new and growing class of anti‐cancer drugs, which decrease oncogene expression by targeting superenhancers. Antibody production is another physiological process relying on superenhancers, and it remains to be clarified whether potential immunomodulatory properties of BET inhibitors might impact humoral immunity and allergy. Methods We thus evaluated humoral immune responses and their Th2 context in vitro and in vivo in mice following treatment with the classical BET‐inhibitor JQ1. We quantified immunoglobulin (Ig) and antibody production by B cells either stimulated in vitro or obtained from immunised mice. JQ1 effects on class switching and activation‐induced deaminase loading were determined, together with modifications of B, T follicular helper (Tfh) and T helper 2 (Th2) populations. JQ1 was finally tested in B‐cell‐dependent models of immune disorders. Results Bromodomain and extra terminal domain inhibition reduced class switching, Ig expression on B cells and antibody secretion and was correlated with decreased numbers of Tfh cells. However, JQ1 strongly increased the proportion of GATA3+ Th2 cells and the secretion of corresponding cytokines. In a mouse allergic model of lung inflammation, JQ1 did not affect eosinophil infiltration or mucus production but enhanced Th2 cytokine production and aggravated clinical manifestations. Conclusion Altogether, BET inhibition thus interweaves intrinsic negative effects on B cells with a parallel complex reshaping of T‐cell polarisation which can increase type 2 cytokines and eventually promote B‐cell‐dependent immunopathology. These opposite and potentially hazardous immunomodulatory effects raise concerns for clinical use of BET inhibitors in patients with immune disorders., While bromodomain and extra terminal domain inhibition reduces class switching, antibody secretion and T follicular helper cell number, this treatment increases the proportion of GATA3+ T helper 2 cells and the secretion of corresponding cytokines. In a mouse model of lung inflammation, JQ1 thus aggravates rather than improves clinical manifestations.

Published
2021
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2. Mesangial deposition can strongly involve innate-like iga molecules lacking affinity maturation

Author

Michel Cogné, Yolla Makhour, Batoul Wehbi, Jeanne Moreau, Anne Druilhe, Christelle Oblet, Arnaud Huard, Etienne Cogné, Marjolein van Egmond, Jean-Claude Aldigier, François Boyer, Bassam Badran, François Paraf, Molecular cell biology and Immunology, Surgery, AGEM - Digestive immunity, AGEM - Re-generation and cancer of the digestive system, AII - Inflammatory diseases, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département Croissance et Signalisation [Paris], 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 Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Limoges (UNILIM), Laboratory of Experimental Hematology, Université libre de Bruxelles (ULB)-Institut Jules Bordet [Bruxelles], Faculté de Médecine [Bruxelles] (ULB), Université libre de Bruxelles (ULB)-Université libre de Bruxelles (ULB)-Faculté de Médecine [Bruxelles] (ULB), Université libre de Bruxelles (ULB), Laboratoire d'Immunologie et Immunopathologie [CHU Poitiers] (CNRS URA 1172), Centre hospitalier universitaire de Poitiers (CHU Poitiers)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM), Université Libre de Bruxelles [Bruxelles] (ULB)-Bordet Institute, Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), and Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, Glycosylation, Antibody Affinity, 030232 urology & nephrology, Inflammation, Receptors, Fc, urologic and male genital diseases, Nephropathy, Affinity maturation, Pathogenesis, Mice, 03 medical and health sciences, 0302 clinical medicine, Antigens, CD, Cytidine Deaminase, Up Front Matters, medicine, Animals, Humans, Receptor, Complement Activation, ComputingMilieux_MISCELLANEOUS, biology, Chemistry, Glomerulonephritis, IGA, General Medicine, medicine.disease, Complement system, Glomerular Mesangium, Immunoglobulin A, Proteinuria, 030104 developmental biology, Basic Research, Nephrology, Mesangium, Immunology, biology.protein, [SDV.IMM]Life Sciences [q-bio]/Immunology, medicine.symptom, Antibody
Abstract

BACKGROUND: IgA nephropathy (IgAN) often follows infections and features IgA mesangial deposition. Polymeric IgA deposits in the mesangium seem to have varied pathogenic potential, but understanding their pathogenicity remains a challenge. Most mesangial IgA1 in human IgAN has a hypogalactosylated hinge region, but it is unclear whether this is required for IgA deposition. Another important question is the role of adaptive IgA responses and high-affinity mature IgA antibodies and whether low-affinity IgA produced by innate-like B cells might also yield mesangial deposits. METHODS: To explore the effects of specific qualitative variations in IgA and whether altered affinity maturation can influence IgA mesangial deposition and activate complement, we used several transgenic human IgA1-producing models with IgA deposition, including one lacking the DNA-editing enzyme activation-induced cytidine deaminase (AID), which is required in affinity maturation. Also, to explore the potential role of the IgA receptor CD89 in glomerular inflammation, we used a model that expresses CD89 in a pattern observed in humans. RESULTS: We found that human IgA induced glomerular damage independent of CD89. When comparing mice able to produce high-affinity IgA antibodies with mice lacking AID-enabled Ig affinity maturation, we found that IgA deposition and complement activation significantly increased and led to IgAN pathogenesis, although without significant proteinuria or hematuria. We also observed that hinge hypoglycosylation was not mandatory for IgA deposition. CONCLUSIONS: In a mouse model of IgAN, compared with high-affinity IgA, low-affinity innate-like IgA, formed in the absence of normal antigen-driven maturation, was more readily involved in IgA glomerular deposition with pathogenic effects.

Published
2019
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3. G-quadruplex DNA targeting alters class-switch recombination in B cells and attenuates allergic inflammation

Author

Brice Laffleur, Dieudonnée Togbe, Jeanne Cook-Moreau, Jean-Claude Aldigier, Iman Dalloul, Valérie F. J. Quesniaux, Zeinab Dalloul, Bernhard Ryffel, Yolla Makhour, Michel Cogné, Jean-Louis Mergny, Pauline Chenuet, François Boyer, Contrôle de la Réponse Immune B et des Lymphoproliférations (CRIBL), Institut Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST), Université de Limoges (UNILIM)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503), Immunologie et Embryologie Moléculaires (IEM), Institut Européen de Chimie et Biologie (IECB), and Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, Dna targeting, Ovalbumin, Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], G-quadruplex, Allergic inflammation, 03 medical and health sciences, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Hypersensitivity, Immunology and Allergy, Animals, ComputingMilieux_MISCELLANEOUS, Cells, Cultured, Inflammation, B-Lymphocytes, Mice, Inbred BALB C, Chemistry, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Allergens, Immunoglobulin Class Switching, Cell biology, G-Quadruplexes, 030104 developmental biology, Immunoglobulin class switching, [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, Acridines, Female
Abstract

International audience

Published
2018
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4. Co and Mn decrease chemical and biological reduction rate of iron oxyhydroxides

Author

Noureddine Bousserrhine, Hiba Noureddine, Mohamad Fakih, Yolla Makhour, and Dana Zeineddine

Subjects
Bacteria, biology, Chemistry, Chemical treatment, Inorganic chemistry, Reduction rate, Biodegradation, Physics and Astronomy(all), biology.organism_classification, biodegradation, soil, Solubilization, Reagent, heavy metals, Dissolution, Clostridium butyricum
Abstract

Very few studies related to the solubilization of Fe (III) oxides substituted by Mn and Co, whereas such oxides are frequent in natural environment. In this present work, goethites substituted for various Mn and Co rates were synthesized and subjected to the reducing action, first, by chemical treatment, with a the dithionite-citratebicarbonate (CBD) reagent, and secondly, by biological treatment with Clostridium butyricum a fermentative Fe (III). The comparison of two processes showed that the dissolution rates of iron decreased with substitution. The study of the bacterial fermentative balance shows that substitution, its rate and its nature, does not influence the bacterial fermentative balance (total activity and number of electron produced were unchanged). However, it decreases the percentage of electrons engaged in the reduction process. This result demonstrates the control of the bacterial reduction of iron oxides by the cristallo-chemical characteristics of the latter.

Published
2011
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6. 198 Identification of a Human Natural Regulatory T Cell Micro-RNA Signature and Demonstration of the Major Role Played by miR-31, miR-21 and Valproate in Foxp3 Expression

Author

Burny Arsène, Badran Bassam, Yolla Makhour, Zeineddine Ibrahim, Martiat Philippe, and Fayyad Kazan Hussein

Subjects
mir-31, Infectious Diseases, Foxp3 expression, medicine.anatomical_structure, Regulatory T cell, microRNA, Immunology, medicine, Pharmacology (medical), Identification (biology), Biology, Cell biology
Published
2011
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