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14 results on '"MESH : Homeostasis"'

1. Homeostasis of Peripheral CD4+ T Cells: IL-2Rα and IL-2 Shape a Population of Regulatory Cells That Controls CD4+ T Cell Numbers

Author

Martine Papiernik, Afonso R. M. Almeida, Antonio A. Freitas, Nicolas Legrand, Biologie des Populations Lymphocytaires, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [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), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), Institut Necker Enfants-Malades (INEM) ( 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 ), Other departments, and Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)

Subjects
CD4-Positive T-Lymphocytes, MESH: Adjuvants, Immunologic, MESH: T-Lymphocyte Subsets, MESH: Mice, Knockout, MESH : Radiation Chimera, Mice, Interleukin 21, 0302 clinical medicine, T-Lymphocyte Subsets, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, Homeostasis, Immunology and Allergy, Cytotoxic T cell, MESH: Animals, IL-2 receptor, MESH: Bone Marrow Transplantation, MESH : Lymphocyte Count, Bone Marrow Transplantation, Mice, Knockout, 0303 health sciences, MESH : Interphase, ZAP70, MESH: CD4-Positive T-Lymphocytes, CD28, Natural killer T cell, Cell biology, MESH: Homeostasis, MESH : CD4-Positive T-Lymphocytes, MESH : Homeostasis, Radiation Chimera, MESH: Survival Analysis, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH : Lymphopenia, MESH: Lymphocyte Count, MESH: Radiation Chimera, Immunology, MESH : Mice, Inbred C57BL, Biology, MESH : Interleukin-2, MESH: Receptors, Interleukin-2, MESH: Interphase, MESH: Lymphopenia, 03 medical and health sciences, Adjuvants, Immunologic, MESH: Mice, Inbred C57BL, MESH : Receptors, Interleukin-2, Lymphopenia, MESH : Mice, Animals, Lymphocyte Count, Antigen-presenting cell, Interphase, MESH: Mice, 030304 developmental biology, Interleukin 3, MESH : Bone Marrow Transplantation, Receptors, Interleukin-2, MESH: Interleukin-2, Survival Analysis, MESH : T-Lymphocyte Subsets, Mice, Inbred C57BL, MESH : Adjuvants, Immunologic, MESH : Mice, Knockout, Interleukin-2, MESH : Animals, MESH : Survival Analysis, 030215 immunology
Abstract

We show that the lymphoid hyperplasia observed in IL-2Rα- and IL-2-deficient mice is due to the lack of a population of regulatory cells essential for CD4 T cell homeostasis. In chimeras reconstituted with bone marrow cells from IL-2Rα-deficient donors, restitution of a population of CD25+CD4+ T cells prevents the chaotic accumulation of lymphoid cells, and rescues the mice from autoimmune disease and death. The reintroduction of IL-2-producing cells in IL-2-deficient chimeras establishes a population of CD25+CD4+ T cells, and restores the peripheral lymphoid compartments to normal. The CD25+CD4+ T cells regulated selectively the number of naive CD4+ T cells transferred into T cell-deficient hosts. The CD25+CD4+/naive CD4 T cell ratio and the sequence of cell transfer determines the homeostatic plateau of CD4+ T cells. Overall, our findings demonstrate that IL-2Rα is an absolute requirement for the development of the regulatory CD25+CD4+ T cells that control peripheral CD4 T cell homeostasis, while IL-2 is required for establishing a sizeable population of these cells in the peripheral pools.

Published
2002
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2. The gut in iron homeostasis: role of HIF-2 under normal and pathological conditions

Author

Maria Mastrogiannaki, Pavle Matak, Carole Peyssonnaux, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Centre National de la Recherche Scientifique (CNRS)-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)-Centre National de la Recherche Scientifique (CNRS), Bos, Mireille, Institut Cochin (UM3 (UMR 8104 / U1016)), and Institut National de la Santé et de la Recherche Médicale (INSERM) - Université Paris Descartes - Paris 5 (UPD5) - Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, MESH: Inflammation, MESH : Basic Helix-Loop-Helix Transcription Factors, MESH: Anoxia, MESH : Hepatocytes, Review Article, Biochemistry, MESH : Iron, Pathogenesis, MESH: Hepatocytes, Mice, MESH: Enterocytes, 0302 clinical medicine, MESH : Hepcidins, MESH: Basic Helix-Loop-Helix Transcription Factors, Basic Helix-Loop-Helix Transcription Factors, Homeostasis, MESH: Animals, MESH: Hepcidins, Hypoxia, Regulation of gene expression, 0303 health sciences, MESH: Iron, MESH : Gene Expression Regulation, MESH: Antimicrobial Cationic Peptides, MESH : Antimicrobial Cationic Peptides, Hematology, MESH : Iron Regulatory Protein 1, MESH : Iron Regulatory Protein 2, MESH: Gene Expression Regulation, MESH : Enterocytes, 3. Good health, Cell biology, MESH : Hemochromatosis, MESH: Homeostasis, MESH : Homeostasis, 030220 oncology & carcinogenesis, Hemochromatosis, medicine.symptom, MESH : Polycythemia, MESH: Hemochromatosis, medicine.medical_specialty, MESH : Anoxia, MESH : Male, Iron, Immunology, Inflammation, Polycythemia, Biology, MESH: Iron Regulatory Protein 1, 03 medical and health sciences, MESH: Iron Regulatory Protein 2, Hepcidins, Hepcidin, Internal medicine, MESH : Mice, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, medicine, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Iron Regulatory Protein 1, Iron Regulatory Protein 2, MESH: Mice, 030304 developmental biology, MESH : Inflammation, MESH: Humans, MESH : Humans, Cell Biology, Hypoxia (medical), medicine.disease, MESH: Male, Gastrointestinal Tract, Enterocytes, Endocrinology, Gene Expression Regulation, Hepatocytes, biology.protein, MESH: Gastrointestinal Tract, MESH : Animals, MESH: Polycythemia, MESH : Gastrointestinal Tract, Antimicrobial Cationic Peptides, Hormone
Abstract

Although earlier, seminal studies demonstrated that the gut per se has the intrinsic ability to regulate the rates of iron absorption, the spotlight in the past decade has been placed on the systemic regulation of iron homeostasis by the hepatic hormone hepcidin and the molecular mechanisms that regulate its expression. Recently, however, attention has returned to the gut based on the finding that hypoxia inducible factor-2 (HIF-2α) regulates the expression of key genes that contribute to iron absorption. Here we review the current understanding of the molecular mechanisms that regulate iron homeostasis in the gut by focusing on the role of HIF-2 under physiological steady-state conditions and in the pathogenesis of iron-related diseases. We also discuss implications for adapting HIF-2–based therapeutic strategies in iron-related pathological conditions.

Published
2013
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3. Arabidopsis thaliana nicotianamine synthase 4 is required for proper response to iron deficiency and to cadmium exposure

Author

Jeremy Astier, Olivier Lamotte, Frédéric Gaymard, Emmanuel Koen, Jossia Boucherez, Angélique Besson-Bard, David Wendehenne, Pierre Richaud, Céline Duc, Antoine Gravot, Agroécologie [Dijon], Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Biochimie et Physiologie Moléculaire des Plantes (BPMP), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Institut National de la Recherche Agronomique (INRA)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro), Amélioration des Plantes et Biotechnologies Végétales (APBV), Institut National de la Recherche Agronomique (INRA)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-AGROCAMPUS OUEST, Bioénergie et Microalgues (EBM), Institut de Biosciences et Biotechnologies d'Aix-Marseille (ex-IBEB) (BIAM), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Agence Nationale de la Recherche [BLAN07-2_184783], University of Burgundy (BQR project), Burgundy State (PARI AGRALE 8 project), French Ministry of Agriculture, Ministere de l'Education Nationale, de la Recherche et de la Technologie, Region Languedoc-Roussillon, Institut National de la Recherche Agronomique, Institut National de la Recherche Agronomique (INRA)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Institut National de la Recherche Agronomique (INRA)-Université de Rennes (UR)-AGROCAMPUS OUEST, Environnement, Bioénergie, Microalgues et Plantes (EBMP), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Université de Montpellier (UM)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro)-Institut National de la Recherche Agronomique (INRA)-Centre National de la Recherche Scientifique (CNRS), AGROCAMPUS OUEST-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Recherche Agronomique (INRA), Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Institut National de la Recherche Agronomique ( INRA ) -Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Biochimie et Physiologie Moléculaire des Plantes ( BPMP ), Centre international d'études supérieures en sciences agronomiques ( Montpellier SupAgro ) -Institut national de la recherche agronomique [Montpellier] ( INRA Montpellier ) -Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut national d’études supérieures agronomiques de Montpellier ( Montpellier SupAgro ), Amélioration des Plantes et Biotechnologies Végétales ( APBV ), Institut National de la Recherche Agronomique ( INRA ) -Université de Rennes 1 ( UR1 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -AGROCAMPUS OUEST, Laboratoire de Bioénergétique et Biotechnologie des Bactéries et Microalgues ( L3BM ), and Commissariat à l'énergie atomique et aux énergies alternatives ( CEA )

Subjects
0106 biological sciences, [ SDV.BV ] Life Sciences [q-bio]/Vegetal Biology, MESH : Azetidinecarboxylic Acid, FMN Reductase, Arabidopsis thaliana, Mutant, Arabidopsis, Gene Expression, Plant Science, 01 natural sciences, MESH : Cation Transport Proteins, MESH : Iron, MESH : Arabidopsis Proteins, Nicotianamine synthase, MESH : Plants, Genetically Modified, chemistry.chemical_compound, MESH : Arabidopsis, Gene Expression Regulation, Plant, Gene expression, MESH: Genes, Plant, MESH : DNA, Bacterial, Homeostasis, MESH: Arabidopsis, Nicotianamine, MESH: Stress, Physiological, Cation Transport Proteins, MESH : Adaptation, Physiological, MESH : Cadmium, 2. Zero hunger, chemistry.chemical_classification, 0303 health sciences, Cadmium, MESH: Iron, biology, General Medicine, Iron Deficiencies, Plants, Genetically Modified, Adaptation, Physiological, MESH: Azetidinecarboxylic Acid, MESH : Phenotype, Phenotype, Biochemistry, MESH: Homeostasis, MESH : Homeostasis, MESH : Mutation, Azetidinecarboxylic Acid, DNA, Bacterial, MESH: Gene Expression, MESH: Mutation, Iron, MESH: Cadmium, chemistry.chemical_element, MESH: Ferritins, MESH: Arabidopsis Proteins, MESH: Alkyl and Aryl Transferases, Genes, Plant, MESH: Phenotype, 03 medical and health sciences, MESH: Cation Transport Proteins, Stress, Physiological, Iron homeostasis, Genetics, [SDV.BV]Life Sciences [q-bio]/Vegetal Biology, Iron deficiency (plant disorder), MESH: Gene Expression Regulation, Plant, MESH : Genes, Plant, MESH : Alkyl and Aryl Transferases, MESH : Stress, Physiological, 030304 developmental biology, MESH : FMN Reductase, Alkyl and Aryl Transferases, Arabidopsis Proteins, Iron deficiency, Nitric oxide, biology.organism_classification, MESH: Adaptation, Physiological, MESH: DNA, Bacterial, MESH : Gene Expression, Enzyme, chemistry, MESH: FMN Reductase, MESH: Plants, Genetically Modified, Ferritins, Mutation, biology.protein, MESH : Ferritins, Agronomy and Crop Science, MESH : Gene Expression Regulation, Plant, 010606 plant biology & botany
Abstract

International audience; The nicotianamine synthase (NAS) enzymes catalyze the formation of nicotianamine (NA), a non-proteinogenic amino acid involved in iron homeostasis. We undertook the functional characterization of AtNAS4, the fourth member of the Arabidopsis thaliana NAS gene family. A mutant carrying a T-DNA insertion in AtNAS4 (atnas4), as well as lines overexpressing AtNAS4 both in the atnas4 and the wild-type genetic backgrounds, were used to decipher the role of AtNAS4 in NA synthesis, iron homeostasis and the plant response to iron deficiency or cadmium supply. We showed that AtNAS4 is an important source for NA. Whereas atnas4 had normal growth in iron-sufficient medium, it displayed a reduced accumulation of ferritins and exhibited a hypersensitivity to iron deficiency. This phenotype was rescued in the complemented lines. Under iron deficiency, atnas4 displayed a lower expression of the iron uptake-related genes IRT1 and FRO2 as well as a reduced ferric reductase activity. Atnas4 plants also showed an enhanced sensitivity to cadmium while the transgenic plants overexpressing AtNAS4 were more tolerant. Collectively, our data, together with recent studies, support the hypothesis that AtNAS4 displays an important role in iron distribution and is required for proper response to iron deficiency and to cadmium supply.

Published
2013
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4. CLIPR-59: a protein essential for neuromuscular junction stability during mouse late embryonic development

Author

Véronique Bernard, Stéphanie Backer, Evelyne Bloch-Gallego, Nathalie Chaverot, Ariane Dimitrov, Jordi Molgó, Franck Perez, Nicolas Offner, Aurélie Couesnon, Institut Cochin (UMR_S567 / UMR 8104), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie des Maladies du Système Nerveux Central, 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), Compartimentation et dynamique cellulaires (CDC), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut Curie [Paris]-Centre National de la Recherche Scientifique (CNRS), Neurobiologie et Développement (N&eD), Centre National de la Recherche Scientifique (CNRS), Institut de Neurobiologie Alfred Fessard (INAF), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Université Pierre et Marie Curie - Paris 6 (UPMC), Neurosciences Paris Seine (NPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), CNRS, Laboratoire de Neurobiologie et Développement, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5), Centre National de la Recherche Scientifique (CNRS)-Institut Curie-Université Pierre et Marie Curie - Paris 6 (UPMC), Université Paris-Sud - Paris 11 (UP11)-Centre National de la Recherche Scientifique (CNRS), Institut Cochin ( UMR_S567 / UMR 8104 ), 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 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 ), Compartimentation et dynamique cellulaires ( CDC ), Centre National de la Recherche Scientifique ( CNRS ) -INSTITUT CURIE-Université Pierre et Marie Curie - Paris 6 ( UPMC ), Neurobiologie et Développement ( N&eD ), Université Paris-Sud - Paris 11 ( UP11 ) -Centre National de la Recherche Scientifique ( CNRS ), Institut de Neurobiologie Alfred Fessard ( INAF ), and Centre National de la Recherche Scientifique ( CNRS )

Subjects
Mutant, MESH: Spinal Cord, Mice, MESH : Embryonic Development, 0302 clinical medicine, MESH: Pregnancy, Pregnancy, MESH: Gestational Age, MESH : Embryo, Mammalian, Homeostasis, MESH: Embryonic Development, MESH : Female, MESH: Animals, Axon, Respiratory system, ComputingMilieux_MISCELLANEOUS, Cells, Cultured, 0303 health sciences, Brain, Anatomy, MESH : Mice, Transgenic, Cell biology, medicine.anatomical_structure, Spinal Cord, MESH: Homeostasis, MESH : Homeostasis, Knockout mouse, Female, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Microtubule-Associated Proteins, MESH: Cells, Cultured, MESH: Mice, Transgenic, Neuromuscular Junction, Embryonic Development, Gestational Age, Mice, Transgenic, MESH : Mice, Inbred C57BL, Biology, Contractility, 03 medical and health sciences, MESH: Brain, MESH: Mice, Inbred C57BL, MESH : Cells, Cultured, MESH : Mice, medicine, Animals, Molecular Biology, MESH: Mice, 030304 developmental biology, Embryogenesis, MESH: Embryo, Mammalian, MESH : Spinal Cord, Embryo, Mammalian, Embryonic stem cell, Mice, Inbred C57BL, MESH : Pregnancy, MESH: Microtubule-Associated Proteins, MESH : Brain, nervous system, MESH : Microtubule-Associated Proteins, [ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH : Neuromuscular Junction, Axon guidance, MESH : Animals, MESH: Neuromuscular Junction, MESH: Female, 030217 neurology & neurosurgery, MESH : Gestational Age, Developmental Biology
Abstract

International audience; CLIPR-59 is a new member of the cytoplasmic linker proteins (CLIP) family mainly localized to the trans-Golgi network. We show here that Clipr-59 expression in mice is restricted to specific pools of neurons, in particular motoneurons (MNs), and progressively increases from embryonic day 12.5 (E12.5) until the first postnatal days. We generated a Clipr-59 knockout mouse model that presents perinatal lethality due to respiratory defects. Physiological experiments revealed that this altered innervation prevents the normal nerve-elicited contraction of the mutant diaphragm that is reduced both in amplitude and fatigue-resistance at E18.5, despite unaffected functional muscular contractility. Innervation of the mutant diaphragm is not altered until E15.5, but is then partially lost in the most distal parts of the muscle. Ultrastructural observations of neuromuscular junctions (NMJs) in the distal region of the diaphragm reveal a normal organization, but a lower density of nerve terminals capped by terminal Schwann cells in E18.5 mutant when compared with control embryos. Similar defects in NMJ stability, with a hierarchy of severity along the caudo-rostral axis, are also observed in other muscles innervated by facial and spinal MNs in Clipr-59 mutant mice. Clipr-59 deficiency therefore affects axon maintenance but not axon guidance toward muscle targets. Thus, CLIPR-59 is involved in the stabilization of specific motor axons at the NMJ during mouse late embryogenesis and its role is crucial for mouse perinatal development.

Published
2013
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5. RANKL induces organized lymph node growth by stromal cell proliferation

Author

S. Lori Bridal, Marion Decossas, Sylvestre Chea, Vincent Duheron, Yongwon Choi, Mattéo R. Bosisio, Frédéric Lézot, Rachel Golub, Christopher G. Mueller, Ariane Berdal, Estelle Hess, Hideo Yagita, Immunologie et chimie thérapeutiques (ICT), Cancéropôle du Grand Est-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie des Adaptations Nutritionnelles (PhAN), Institut National de la Recherche Agronomique (INRA)-Université de Nantes (UN), Lymphopoïèse, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'Imagerie Paramétrique (LIP), Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR58-Centre National de la Recherche Scientifique (CNRS), ECHOSENS S.A., Echosens, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Department of Immunology, Juntendo University School of Medicine, Physiopathologie de la Résorption Osseuse et Thérapie des Tumeurs Osseuses Primitives, Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Pennsylvania [Philadelphia], Immunologie et chimie thérapeutiques ( ICT ), Cancéropôle du Grand Est-Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -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 Nantes ( UN ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Laboratoire d'Imagerie Paramétrique ( LIP ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -IFR58-Centre National de la Recherche Scientifique ( CNRS ), Université Paris Descartes - Paris 5 (UPD5)-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), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)

Subjects
MESH: Chemokine CCL19, MESH: Lymph Nodes, MESH : Hair Follicle, Mice, 0302 clinical medicine, MESH : Cell Proliferation, Homeostasis, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, Immunology and Allergy, MESH: Animals, Lymph node, MESH : Lymph Nodes, 0303 health sciences, MESH: RANK Ligand, MESH : Mice, Transgenic, MESH : Chemokine CXCL13, Cell biology, medicine.anatomical_structure, Lymphatic system, RANKL, MESH: Homeostasis, MESH : Homeostasis, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Hair Follicle, MESH : RANK Ligand, MESH: Chemokine CXCL13, Hair Follicle, Stromal cell, MESH: Mice, Transgenic, Immunology, Mice, Transgenic, Biology, 03 medical and health sciences, MESH: Cell Proliferation, MESH : Mice, medicine, Lymph node stromal cell, Animals, CXCL13, MESH: Mice, B cell, Cell Proliferation, 030304 developmental biology, MESH: Immune System, RANK Ligand, Hair follicle, Chemokine CXCL13, MESH : Chemokine CCL19, Immune System, MESH : Stromal Cells, MESH : Immune System, biology.protein, Chemokine CCL19, Lymph Nodes, MESH : Animals, Stromal Cells, MESH: Stromal Cells, 030215 immunology
Abstract

RANK and its ligand RANKL play important roles in the development and regulation of the immune system. We show that mice transgenic for Rank in hair follicles display massive postnatal growth of skin-draining lymph nodes. The proportions of hematopoietic and nonhematopoietic stromal cells and their organization are maintained, with the exception of an increase in B cell follicles. The hematopoietic cells are not activated and respond to immunization by foreign Ag and adjuvant. We demonstrate that soluble RANKL is overproduced from the transgenic hair follicles and that its neutralization normalizes lymph node size, inclusive area, and numbers of B cell follicles. Reticular fibroblastic and vascular stromal cells, important for secondary lymphoid organ formation and organization, express RANK and undergo hyperproliferation, which is abrogated by RANKL neutralization. In addition, they express higher levels of CXCL13 and CCL19 chemokines, as well as MAdCAM-1 and VCAM-1 cell-adhesion molecules. These findings highlight the importance of tissue-derived cues for secondary lymphoid organ homeostasis and identify RANKL as a key molecule for controlling the plasticity of the immune system.

Published
2012
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6. 24S-hydroxycholesterol and cholesterol-24S-hydroxylase (CYP46A1) in the retina: from cholesterol homeostasis to pathophysiology of glaucoma

Author

Niyazi Acar, Catherine Creuzot-Garcher, Alain M. Bron, Cynthia Fourgeux, Lionel Bretillon, Centre des Sciences du Goût et de l'Alimentation [Dijon] ( CSGA ), Institut National de la Recherche Agronomique ( INRA ) -Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique ( CNRS ), Service d'Ophtalmologie (CHU de Dijon), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Centre des Sciences du Goût et de l'Alimentation [Dijon] (CSGA), Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), and Centre National de la Recherche Scientifique (CNRS)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)

Subjects
genetic structures, [SDV]Life Sciences [q-bio], Glaucoma, Biochemistry, chemistry.chemical_compound, MESH: Hydroxycholesterols, MESH : Hydroxycholesterols, 0302 clinical medicine, Homeostasis, MESH: Animals, MESH : Glaucoma, 0303 health sciences, MESH: Retina, Pathophysiology, 3. Good health, medicine.anatomical_structure, Cholesterol, MESH: Homeostasis, MESH : Homeostasis, lipids (amino acids, peptides, and proteins), MESH: Glaucoma, MESH: Steroid Hydroxylases, medicine.medical_specialty, Biology, Retinal ganglion, Retina, 03 medical and health sciences, Internal medicine, medicine, Cholesterol 24-Hydroxylase, Animals, Humans, Cholesterol 24-hydroxylase, Molecular Biology, 030304 developmental biology, MESH : Steroid Hydroxylases, MESH: Humans, [ SDV ] Life Sciences [q-bio], Organic Chemistry, MESH : Humans, MESH : Retina, Cell Biology, Neuron, medicine.disease, Hydroxycholesterols, eye diseases, Endocrinology, Metabolism, chemistry, Steroid Hydroxylases, sense organs, MESH : Animals, 030217 neurology & neurosurgery
Abstract

http://www.sciencedirect.com/; International audience; Free cholesterol is the predominant form of cholesterol in the neural retina. The vertebrate neural retina exhibits its own capacity to synthesize cholesterol and meets its demand also by taking it from the circulation. Defects in cholesterol synthesis and trafficking in the neural retina has detrimental consequences on its structure and function, highlighting the crucial importance of maintaining cholesterol homeostasis in the retina. Our purpose was to give a review on the functioning of the retina, the role of cholesterol and cholesterol metabolism therein, with special emphasis on cholesterol-24S-hydroxylase (CYP46A1). Similar to the brain, the retina expresses cholesterol-24S-hydroxylase (CYP46A1) and is enriched in its metabolic product, 24S-hydroxycholesterol. We recently published that one single nucleotide polymorphism in CYP46A1 gene, designated as rs754203, was a risk factor for glaucoma. Glaucoma is the second leading cause of blindness worldwide, affecting more than 60 million people. Glaucoma is characterized by the loss of retinal ganglion cells, which show high CYP46A1 expression. These data suggest the potential involvement of CYP46A1 and 24S-hydroxycholesterol in the pathophysiology of glaucoma.

Published
2011
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7. AMP-activated protein kinase in the regulation of hepatic energy metabolism: from physiology to therapeutic perspectives.: AMPK in the liver

Author

Benoit Viollet, Marc Foretz, Sophie Hébrard, Fabrizio Andreelli, Bruno Guigas, Rémi Mounier, Jocelyne Leclerc, Louise Lantier, Institut Cochin (UMR_S567 / UMR 8104), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Division of cardiology, Université Catholique de Louvain (UCL), Department of Molecular Cell Biology, Leiden University Medical Center (LUMC), Déterminants génétiques du diabète de type 2 et de ses complications vasculaires, Université Paris Diderot - Paris 7 (UPD7) - Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Diabétologie-Endocrinologie-Nutrition, Assistance publique - Hôpitaux de Paris (AP-HP) - AP-HP - Hôpital Bichat - Claude Bernard [Paris] - Université Paris Diderot - Paris 7 (UPD7), FP6 EXGENESIS Integrated Project (LSHM-CT- 2004-005272), PNRD, ALFEDIAM, Institut Benjamin Delessert., 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 Catholique de Louvain = Catholic University of Louvain (UCL), Déterminants génétiques du diabète de type 2 et de ses complications vasculaires ((U 695)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Université Paris Diderot - Paris 7 (UPD7)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
Liver Cirrhosis, MESH : Ribonucleotides, MESH : Fatty Liver, Physiology, Protein Conformation, MESH : Protein Subunits, MESH : Dyslipidemias, AMP-Activated Protein Kinases, 0302 clinical medicine, MESH: Protein Conformation, AMP-activated protein kinase, MESH : Lipid Metabolism, energy metabolism, Glucose homeostasis, Homeostasis, MESH: Animals, MESH: AMP-Activated Protein Kinases, Beta oxidation, MESH: Fatty Liver, MESH : Protein Conformation, MESH: Lipid Metabolism, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, 0303 health sciences, biology, MESH: Energy Metabolism, MESH: Gluconeogenesis, hepatic glucose production, MESH : AMP-Activated Protein Kinases, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, MESH: Protein Subunits, Mitochondria, MESH: Glucose, MP-activated protein kinase, MESH: Homeostasis, 030220 oncology & carcinogenesis, MESH : Homeostasis, Lipogenesis, MESH : Aminoimidazole Carboxamide, type 2 diabetes, MESH : Mitochondria, MESH: Liver Cirrhosis, medicine.medical_specialty, MESH: Mitochondria, MESH : Gluconeogenesis, Carbohydrate metabolism, MESH: Aminoimidazole Carboxamide, liver, Article, 03 medical and health sciences, Internal medicine, MESH: Hypoglycemic Agents, medicine, Animals, Humans, Hypoglycemic Agents, MESH : Liver Cirrhosis, 030304 developmental biology, Dyslipidemias, fatty liver, MESH: Humans, MESH : Glucose, MESH: Dyslipidemias, MESH : Humans, Gluconeogenesis, AMPK, MESH : Liver, Lipid metabolism, Ribonucleotides, Aminoimidazole Carboxamide, Lipid Metabolism, MESH : Hypoglycemic Agents, MESH : Energy Metabolism, Protein Subunits, therapeutic, Endocrinology, Glucose, MESH: Ribonucleotides, Mitochondrial biogenesis, biology.protein, MESH : Animals, MESH: Liver
Abstract

International audience; As the liver is central in the maintenance of glucose homeostasis and energy storage, knowledge of the physiology as well as physiopathology of hepatic energy metabolism is a prerequisite to our understanding of whole-body metabolism. Hepatic fuel metabolism changes considerably depending on physiological circumstances (fed vs. fasted state). In consequence, hepatic carbohydrate, lipid and protein synthesis/utilization are tightly regulated according to needs. Fatty liver and hepatic insulin resistance (both frequently associated with the metabolic syndrome) or increased hepatic glucose production (as observed in type 2 diabetes) resulted from alterations in substrates oxidation/storage balance in the liver. Because AMP-activated protein kinase (AMPK) is considered as a cellular energy sensor, it is important to gain understanding of the mechanism by which hepatic AMPK coordinates hepatic energy metabolism. AMPK has been implicated as a key regulator of physiological energy dynamics by limiting anabolic pathways (to prevent further ATP consumption) and by facilitating catabolic pathways (to increase ATP generation). Activation of hepatic AMPK leads to increased fatty acid oxidation and simultaneously inhibition of hepatic lipogenesis, cholesterol synthesis and glucose production. In addition to a short-term effect on specific enzymes, AMPK also modulates the transcription of genes involved in lipogenesis and mitochondrial biogenesis. The identification of AMPK targets in hepatic metabolism should be useful in developing treatments to reverse metabolic abnormalities of type 2 diabetes and the metabolic syndrome.

Published
2009
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8. Inflammation and oxidative stress in vertebrate host-parasite systems

Author

Sorci , Gabriele, Faivre , Bruno, Biogéosciences [Dijon] ( BGS ), and Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique ( CNRS )

Subjects
MESH : Oxidative Stress, [ SDE.BE ] Environmental Sciences/Biodiversity and Ecology, MESH : Inflammation, MESH : Host-Parasite Interactions, MESH : Humans, MESH : Reactive Oxygen Species, MESH : Immunity, Innate, delayed costs, [ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology, MESH : Aging, ageing, nitric oxide, MESH : Homeostasis, MESH : Selection (Genetics), MESH : Animals, innate immunity, MESH : Reactive Nitrogen Species, reactive oxygen and nitrogen species, immune evasion
Abstract

13 pages; International audience; Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms. Inflammation relies on a number of cellular and molecular effectors that can strike invading pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-specific way. Owing to this non-specific response, inflammation can generate substantial costs for the host if the inflammatory response, and the associated oxygen-based damage, get out of control. This imposes strong selection pressure that acts to optimize two key features of the inflammatory response: the timing of activation and resolution (the process of downregulation of the response). In this paper, we review the benefits and costs of inflammation-driven immunity. Our aim is to emphasize the importance of resolution of inflammation as a way of maintaining homeostasis against oxidative stress and to prevent the 'horror autotoxicus' of chronic inflammation. Nevertheless, host immune regulation also opens the way to pathogens to subvert host defences. Therefore, quantifying inflammatory costs requires assessing (i) short-term negative effects, (ii) delayed inflammation-driven diseases, and (iii) parasitic strategies to subvert inflammation.

Published
2009
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9. [Reactive oxygen species, stress and cell death in plants]

Author

Parent , Claire, Capelli , Nicolas, Dat , James, Laboratoire Chrono-environnement - CNRS - UBFC (UMR 6249) (LCE), Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Laboratoire Chrono-environnement ( LCE ), and Université Bourgogne Franche-Comté ( UBFC ) -Université de Franche-Comté ( UFC ) -Centre National de la Recherche Scientifique ( CNRS )

Subjects
MESH: Cell Death, MESH: Oxidation-Reduction, MESH: Plants, MESH : Reactive Oxygen Species, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Environment, MESH : Plants, MESH : Plant Leaves, Plant Cells, Homeostasis, MESH : Plant Physiological Phenomena, MESH: Environment, Plant Physiological Phenomena, MESH : Oxidation-Reduction, Cell Death, [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, MESH: Plant Physiological Phenomena, MESH: Reactive Oxygen Species, MESH : Environment, Plant Leaves, MESH: Plant Leaves, MESH: Homeostasis, MESH : Cell Death, MESH : Homeostasis, Reactive Oxygen Species, Oxidation-Reduction
Abstract

International audience; Plants are constantly exposed to changes in environmental conditions. During periods of stress, the cellular redox homeostasis is altered as a result of reactive oxygen species accumulation. The change in redox is responsible for the symptoms commonly observed during periods of stress and reflects the phytotoxic nature of oxygen radical accumulation. However, oxygen radicals have recently been identified as key actors in the response to stress and their role as secondary messengers is now clearly established. The identification of their role in gene regulation has allowed one to identify them as key regulators in the induction and execution of programmed cell death typically observed during developmental processes as well as during stress responses. This review presents recent advances in the characterisation of the role of reactive oxygen species in plants.

Published
2008
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10. AMP-activated protein kinase alpha2 deficiency affects cardiac cardiolipin homeostasis and mitochondrial function

Author

Philippe Mateo, Sophie Vaulont, Vladimir Veksler, James R. Wilding, Renée Ventura-Clapier, Marta Novotova, J. A. Hoerter, Alain Grynberg, Delphine Rousseau, Yoni Athéa, Anne Garnier, Benoit Viollet, Signalisation et physiopathologie cardiaque, Université Paris-Sud - Paris 11 (UP11) - IFR141 - Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Cochin (UMR_S567 / UMR 8104), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Nutrition Lipidique et Régulation Fonctionnelle du Cœur et des Vaisseaux (UMR INRA 1154), Institut National de la Recherche Agronomique (INRA) - Université Paris-Sud - Paris 11 (UP11) - IFR141, Institute of Molecular Physiology and Genetics (IMPG), Slovak Academy of Science [Bratislava] (SAS), and This work was supported by the 'Association Française contre les Myopathies' and 'Fondation de France', the European Commission FP6 program (EXGENESIS-Grant QLG1-CT-2001-01488), and the European Union Contract (LSHM-CT-2005-018833/EUGeneHeart). The Franco-Slovak collaboration was funded by a French STEFANIK grant and by Slovak VEGA 2/6079/26 and APVT-51-31104.

Subjects
Male, AMPK, Endocrinology, Diabetes and Metabolism, Respiratory chain, MESH : Gene Deletion, AMP-Activated Protein Kinases, 030204 cardiovascular system & hematology, Mitochondrion, Mitochondria, Heart, Mice, chemistry.chemical_compound, 0302 clinical medicine, AMP-activated protein kinase, Cardiolipin, complex-I, MESH : Myocardium, Homeostasis, Myocytes, Cardiac, MESH : Oleic Acid, Inner mitochondrial membrane, MESH : Fatty Acids, Phospholipids, Heart metabolism, 0303 health sciences, biology, cardiolipins, MESH : Multienzyme Complexes, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, mitochondria, Biochemistry, MESH : Homeostasis, MESH : Cardiolipins, MESH : Male, MESH : Myocytes, Cardiac, Protein Serine-Threonine Kinases, fatty acids, Article, Gene Expression Regulation, Enzymologic, MESH : Phospholipids, MESH : Gene Expression Regulation, Enzymologic, 03 medical and health sciences, Multienzyme Complexes, MESH : Mice, Internal Medicine, Animals, Protein kinase A, 030304 developmental biology, MESH : Glucose, Myocardium, MESH : Protein, MESH : Energy Metabolism, Glucose, chemistry, biology.protein, MESH : Animals, MESH : Mitochondria, Heart, Energy Metabolism, Gene Deletion, respiration, Oleic Acid
Abstract

AMP-activated protein kinase (AMPK) plays an important role in controlling energy homeostasis and is envisioned as a promising target to treat metabolic disorders. In the heart, AMPK is involved in short-term regulation and in transcriptional control of proteins involved in energy metabolism. Here, we investigated whether deletion of AMPKalpha2, the main cardiac catalytic isoform, alters mitochondrial function and biogenesis. Body weight, heart weight, and AMPKalpha1 expression were similar in control littermate and AMPKalpha2(-/-) mice. Despite normal oxygen consumption in perfused hearts, maximal oxidative capacity, measured using saponin permeabilized cardiac fibers, was approximately 30% lower in AMPKalpha2(-/-) mice with octanoate, pyruvate, or glutamate plus malate but not with succinate as substrates, showing an impairment at complex I of the respiratory chain. This effect was associated with a 25% decrease in mitochondrial cardiolipin content, the main mitochondrial membrane phospholipid that is crucial for complex I activity, and with a 13% decrease in mitochondrial content of linoleic acid, the main fatty acid of cardiolipins. The decrease in cardiolipin content could be explained by mRNA downregulation of rate-limiting enzymes of both cardiolipin synthesis (CTP:PA cytidylyltransferase) and remodeling (acyl-CoA:lysocardiolipin acyltransferase 1). These data reveal a new role for AMPKalpha2 subunit in the regulation of cardiac muscle oxidative capacity via cardiolipin homeostasis.

Published
2007
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11. Control of blood cell homeostasis in Drosophila larvae by the posterior signalling centre

Author

Laurence Dubois, Michèle Crozatier, Rami Makki, Alain Vincent, Joanna Krzemień, Marie Meister, Centre de biologie du développement (CBD), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Département de Recherche sur l'Etat Condensé, les Atomes et les Molécules (DRECAM), Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Institut d’Électronique, de Microélectronique et de Nanotechnologie (IEMN) - UMR 8520 (IEMN), Centre National de la Recherche Scientifique (CNRS)-Université de Lille-Université Polytechnique Hauts-de-France (UPHF)-Ecole Centrale de Lille-Université Polytechnique Hauts-de-France (UPHF)-Institut supérieur de l'électronique et du numérique (ISEN), Réponse immunitaire et developpement chez les insectes (RIDI - UPR 9002), Université de Strasbourg (UNISTRA)-Institut de biologie moléculaire et cellulaire (IBMC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Fakultät für Ingenieurwissenschaften und Informatik, Universität Ulm - Ulm University [Ulm, Allemagne], Laboratoire Bordelais de Recherche en Informatique (LaBRI), Centre National de la Recherche Scientifique (CNRS)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB)-Université Sciences et Technologies - Bordeaux 1-Université Bordeaux Segalen - Bordeaux 2, Institut de Génomique Fonctionnelle (IGF), Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Anatomopathologie Haut-Lévêque (ANATOMOPATHOLOGIE), CHU, Clinical Neurology Oxford (CLINICAL NEUROLOGY), Hospital, Departement /u661 : Endocrinologie, Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de synthèse organique (DCSO), École polytechnique (X)-Centre National de la Recherche Scientifique (CNRS), FLAveur, VIsion et Comportement du consommateur (FLAVIC), Etablissement National d'Enseignement Supérieur Agronomique de Dijon (ENESAD)-Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Centre de Biologie Intégrative (CBI), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN), Centrale Lille-Institut supérieur de l'électronique et du numérique (ISEN)-Université de Valenciennes et du Hainaut-Cambrésis (UVHC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF), Institut de biologie moléculaire et cellulaire (IBMC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-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), Université de Bordeaux (UB)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB)-Centre National de la Recherche Scientifique (CNRS), École polytechnique (X)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre de Biologie Intégrative (CBI), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS)-École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB), Institut National de la Recherche Agronomique (INRA)-Etablissement National d'Enseignement Supérieur Agronomique de Dijon (ENESAD)-Université de Bourgogne (UB), Centre de biologie du développement ( CBD ), Université Paul Sabatier - Toulouse 3 ( UPS ) -Centre National de la Recherche Scientifique ( CNRS ), Département de Recherche sur l'Etat Condensé, les Atomes et les Molécules ( DRECAM ), Commissariat à l'énergie atomique et aux énergies alternatives ( CEA ), Institut d’Électronique, de Microélectronique et de Nanotechnologie (IEMN) - UMR 8520 ( IEMN ), Ecole Centrale de Lille-Institut supérieur de l'électronique et du nunérique (ISEN)-Université de Valenciennes et du Hainaut-Cambresis ( UVHC ) -Université de Lille-Centre National de la Recherche Scientifique ( CNRS ), Réponse immunitaire et developpement chez les insectes ( RIDI - UPR 9002 ), Institut de biologie moléculaire et cellulaire ( IBMC ), Université de Strasbourg ( UNISTRA ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Strasbourg ( UNISTRA ) -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 ), Universität Ulm, Laboratoire Bordelais de Recherche en Informatique ( LaBRI ), Centre National de la Recherche Scientifique ( CNRS ) -École Nationale Supérieure d'Électronique, Informatique et Radiocommunications de Bordeaux (ENSEIRB)-Université Sciences et Technologies - Bordeaux 1-Université Bordeaux Segalen - Bordeaux 2, Institut de Génomique Fonctionnelle ( IGF ), Centre National de la Recherche Scientifique ( CNRS ) -Université Montpellier 2 - Sciences et Techniques ( UM2 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Montpellier 1 ( UM1 ) -Université de Montpellier ( UM ), Anatomopathologie Haut-Lévêque ( ANATOMOPATHOLOGIE ), Clinical Neurology Oxford ( CLINICAL NEUROLOGY ), Université Montpellier 1 ( UM1 ) -Université Montpellier 2 - Sciences et Techniques ( UM2 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Laboratoire de synthèse organique ( DCSO ), École polytechnique ( X ) -Centre National de la Recherche Scientifique ( CNRS ), FLAveur, VIsion et Comportement du consommateur ( FLAVIC ), and Etablissement National d'Enseignement Supérieur Agronomique de Dijon ( ENESAD ) -Institut National de la Recherche Agronomique ( INRA ) -Université de Bourgogne ( UB )

Subjects
MESH: Signal Transduction, Cellular immunity, Hemocytes, Cellular differentiation, Wasps, Hemocyte differentiation, MESH: Hematopoiesis, MESH : Janus Kinases, MESH: Hematopoietic Stem Cells, Blood cell, 0302 clinical medicine, MESH : Drosophila melanogaster, MESH: Janus Kinases, Homeostasis, MESH: Animals, 0303 health sciences, Multidisciplinary, Cell Differentiation, MESH : Wasps, Cell biology, Haematopoiesis, STAT Transcription Factors, medicine.anatomical_structure, Drosophila melanogaster, MESH: Homeostasis, MESH : Homeostasis, Larva, MESH: Wasps, MESH : Cell Differentiation, Signal Transduction, MESH: Cell Differentiation, MESH: Lymphatic System, Notch signaling pathway, Biology, MESH: Drosophila melanogaster, Lymphatic System, 03 medical and health sciences, medicine, Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, 030304 developmental biology, Janus Kinases, MESH : Signal Transduction, MESH : Lymphatic System, Innate immune system, MESH : Larva, MESH : Hematopoietic Stem Cells, MESH: Hemocytes, MESH : STAT Transcription Factors, Lamellocyte differentiation, MESH: STAT Transcription Factors, Hematopoietic Stem Cells, Hematopoiesis, MESH : Hematopoiesis, Immunology, MESH : Animals, MESH : Hemocytes, MESH: Larva, 030217 neurology & neurosurgery
Abstract

Drosophila haemocytes (blood cells) originate from a specialized haematopoietic organ-the lymph gland. Larval haematopoietic progenitors (prohaemocytes) give rise to three types of circulating haemocytes: plasmatocytes, crystal cells and lamellocytes. Lamellocytes, which are devoted to encapsulation of large foreign bodies, only differentiate in response to specific immune threats, such as parasitization by wasps. Here we show that a small cluster of signalling cells, termed the PSC (posterior signalling centre), controls the balance between multipotent prohaemocytes and differentiating haemocytes, and is necessary for the massive differentiation of lamellocytes that follows parasitization. Communication between the PSC and haematopoietic progenitors strictly depends on the PSC-restricted expression of Collier, the Drosophila orthologue of mammalian early B-cell factor. PSC cells act, in a non-cell-autonomous manner, to maintain JAK/STAT signalling activity in prohaemocytes, preventing their premature differentiation. Serrate-mediated Notch signalling from the PSC is required to maintain normal levels of col transcription. The key role of the PSC in controlling blood cell homeostasis is reminiscent of interactions between haematopoietic progenitors and their micro-environment in vertebrates, thus further highlighting the interest of Drosophila as a model system for studying the evolution of haematopoiesis and cellular innate immunity.

Published
2006
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12. Adenovirus-mediated overexpression of sterol regulatory element binding protein-1c mimics insulin effects on hepatic gene expression and glucose homeostasis in diabetic mice

Author

Isabelle Hainault, Dalila Azzout-Marniche, Pascal Ferré, Lydia Bertry-Coussot, Dominique Bécard, Fabienne Foufelle, Physiologie de la Nutrition et du Comportement Alimentaire ( PNCA ), Institut National de la Recherche Agronomique ( INRA ) -AgroParisTech, Centre de Recherche des Cordeliers ( CRC ), Université Paris Diderot - Paris 7 ( UPD7 ) -École pratique des hautes études ( EPHE ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Physiologie de la Nutrition et du Comportement Alimentaire (PNCA), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Azzout-Marniche, Dalila, AgroParisTech-Institut National de la Recherche Agronomique (INRA), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE)

Subjects
Male, MESH : RNA, Messenger, [SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], MESH: CCAAT-Enhancer-Binding Proteins, MESH: Recombinant Proteins, Mice, 0302 clinical medicine, Homeostasis, Insulin, Glucose homeostasis, MESH: Animals, 0303 health sciences, MESH: Mice, Inbred CBA, Glycogen, Gene Transfer Techniques, MESH: Adenoviridae, [SDV.BBM.MN]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], MESH: Transcription Factors, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, MESH : Genetic Vectors, 3. Good health, MESH : DNA-Binding Proteins, MESH : Diabetes Mellitus, Experimental, Sterol Regulatory Element Binding Protein 1, medicine.medical_specialty, MESH: Gene Expression, MESH: Gene Transfer Techniques, MESH: Insulin, [ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Adenoviridae, MESH: Sterol Regulatory Element Binding Protein 1, 03 medical and health sciences, MESH : Sterol Regulatory Element Binding Protein 1, [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], RNA, Messenger, MESH : Gene Transfer Techniques, MESH : Injections, Intraperitoneal, MESH : Glucose, Glucokinase, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, medicine.disease, MESH : Gene Expression, Glucose, Endocrinology, [SDV.BBM.MN] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], chemistry, CCAAT-Enhancer-Binding Proteins, Mice, Inbred CBA, MESH: Liver, Transcription Factors, MESH : Transcription Factors, MESH : Insulin, MESH : Mice, Inbred CBA, [ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition, Gene Expression, [SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], [SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, chemistry.chemical_compound, MESH: Genetic Vectors, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], MESH: Diabetes Mellitus, Experimental, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [ SDV.MHEP.PHY ] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Recombinant Proteins, MESH: Glucose, DNA-Binding Proteins, Liver, MESH : CCAAT-Enhancer-Binding Proteins, MESH: Homeostasis, MESH : Homeostasis, Phosphoenolpyruvate carboxykinase, MESH: Injections, Intraperitoneal, Injections, Intraperitoneal, MESH : Recombinant Proteins, MESH : Male, Genetic Vectors, 030209 endocrinology & metabolism, Biology, Diabetes Mellitus, Experimental, [ SDV.BC.IC ] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], [ SDV.BBM.MN ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], Diabetes mellitus, Internal medicine, MESH : Mice, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Internal Medicine, medicine, Animals, MESH : Adenoviridae, MESH: Mice, Transcription factor, MESH: RNA, Messenger, 030304 developmental biology, [ SDV.BC.BC ] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], MESH : Liver, Metabolism, MESH: Male, [SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, MESH : Animals, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, MESH: DNA-Binding Proteins
Abstract

International audience; In vitro, the transcription factor sterol regulatory element binding protein-1c (SREBP-1c) mimics the positive effects of insulin on hepatic genes involved in glucose utilization, such as glucokinase (GK) and enzymes of the lipogenic pathway, suggesting that it is a key factor in the control of hepatic glucose metabolism. Decreased glucose utilization and increased glucose production by the liver play an important role in the development of the hyperglycemia in diabetic states. We thus reasoned that if SREBP-1c is indeed a mediator of hepatic insulin action, a hepatic targeted overexpression of SREBP-1c should greatly improve glucose homeostasis in diabetic mice. This was achieved by injecting streptozotocin-induced diabetic mice with a recombinant adenovirus containing the cDNA of the mature, transcriptionally active form of SREBP-1c. We show here that overexpressing SREBP-1c specifically in the liver of diabetic mice induces GK and lipogenic enzyme gene expression and represses the expression of phosphoenolpyruvate carboxykinase, a key enzyme of the gluconeogenic pathway. This in turn increases glycogen and triglyceride hepatic content and leads to a marked decrease in hyperglycemia in diabetic mice. We conclude that SREBP-1c has a major role in vivo in the long-term control of glucose homeostasis by insulin.

Published
2001

13. Sterol-regulatory-element-binding protein 1c mediates insulin action on hepatic gene expression

Author

Ferré, P., Foretz, F, Azzout-Marniche, Dalila, Bécard, D, Foufelle, F., Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), [Institut Cochin] Département Endocrinologie, métabolisme, diabète (EMD) (EMD), Institut Cochin (IC UM3 (UMR 8104 / U1016)), 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 Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers ( CRC ), Université Paris Diderot - Paris 7 ( UPD7 ) -École pratique des hautes études ( EPHE ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), [Institut Cochin] Département Endocrinologie, métabolisme, diabète (EMD) ( EMD ), Institut Cochin ( UM3 (UMR 8104 / U1016) ), and 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 )

Subjects
MESH : Transcription Factors, MESH : Insulin, [ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], MESH: CCAAT-Enhancer-Binding Proteins, MESH : Mammals, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Homeostasis, Insulin, MESH: Animals, MESH : Glycolysis, Mammals, MESH : Gene Expression Regulation, MESH : Glucagon, [ SDV.MHEP.PHY ] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], MESH: Glucagon, MESH: Energy Metabolism, [SDV.BBM.MN]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], MESH: Transcription Factors, [ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, MESH: Gene Expression Regulation, MESH: Glucose, DNA-Binding Proteins, MESH : CCAAT-Enhancer-Binding Proteins, Liver, MESH: Homeostasis, MESH : Homeostasis, MESH: Glycolysis, MESH : DNA-Binding Proteins, Sterol Regulatory Element Binding Protein 1, Glycolysis, [ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, MESH: Insulin, MESH: Mammals, [ SDV.BC.IC ] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], [ SDV.BBM.MN ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], MESH: Sterol Regulatory Element Binding Protein 1, MESH : Sterol Regulatory Element Binding Protein 1, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], Animals, MESH : Glucose, [ SDV.BC.BC ] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], MESH : Liver, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Glucagon, MESH : Energy Metabolism, Glucose, Gene Expression Regulation, CCAAT-Enhancer-Binding Proteins, MESH : Animals, Energy Metabolism, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, MESH: DNA-Binding Proteins, MESH: Liver, Transcription Factors
Abstract

International audience; Effects of insulin on the expression of liver-specific genes are part of the adaptive mechanisms aimed at maintaining energy homeostasis in mammals. When the diet is rich in carbohydrates, secreted insulin stimulates the expression of genes for enzymes involved in glucose utilization (glucokinase, L-type pyruvate kinase and lipogenic enzymes) and inhibits genes for enzymes involved in glucose production (phosphenolpyruvate carboxykinase). The mechanisms by which insulin controls the expression of these genes have been poorly understood. Recently, the transcription factor sterol-regulatory-element-binding protein 1c has been proposed as a key mediator of insulin transcriptional effects. Here we review the evidence that has led to this proposal and the consequences for our understanding of insulin effects in physiological or pathological conditions.

Published
2001

14. Lymphocyte homeostasis

Author

Corinne Tanchot, Manuela M. Rosado, Fabien Agenes, Antonio A. Freitas, Benedita Rocha, 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), Dynamiques Lymphocytaires, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Institut Necker Enfants-Malades (INEM) ( 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 ), and Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS )

Subjects
MESH : Immunologic Memory, T-Lymphocytes, Immunology, Bone Marrow Cells, Thymus Gland, MESH : Models, Immunological, Lymphocyte Activation, MESH: Models, Immunological, MESH : B-Lymphocytes, 03 medical and health sciences, Mice, 0302 clinical medicine, MESH: B-Lymphocytes, MESH : Mice, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, Immunology and Allergy, Animals, Homeostasis, MESH : Thymus Gland, MESH: Animals, MESH: Lymphocyte Activation, MESH: Mice, MESH : Lymphocyte Activation, 030304 developmental biology, MESH : T-Lymphocytes, 0303 health sciences, B-Lymphocytes, MESH: Bone Marrow Cells, Models, Immunological, MESH: Thymus Gland, MESH: T-Lymphocytes, MESH: Homeostasis, MESH : Homeostasis, MESH: Immunologic Memory, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH : Animals, Immunologic Memory, MESH : Bone Marrow Cells, 030215 immunology
Abstract

International audience; B- and T-lymphocyte populations have an independent homeostatic regulation of resting (B and T) and activated (B) or memory (T) cell compartments. This organization may provide an efficient mechanism to ensure simultaneously a first natural barrier of protection against common pathogens, the maintenance of immunological T-cell memory and a reservoir of repertoire diversity capable of dealing with new antigenic challenges.

Published
1997
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