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1. Virtual Memory CD8+ T Cells: Origin and Beyond

Author

Maria Estefania Viano, Natalia Soledad Baez, Constanza Savid-Frontera, Nicolás Leonel Lidon, Deborah L. Hodge, André Herbelin, Jean-Marc Gombert, Alice Barbarin, Maria Cecilia Rodriguez-Galan, Universidad Nacional de Córdoba [Argentina], National Institutes of Health [Bethesda] (NIH), Ischémie Reperfusion, Métabolisme et Inflammation Stérile en Transplantation (IRMETIST), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'immunologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), and Barbarin, Alice

Subjects
[SDV.IMM] Life Sciences [q-bio]/Immunology, Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Cell Biology, infection, human TVM cells, [SDV.CAN] Life Sciences [q-bio]/Cancer, Virology, Ag-specific T cells, cancer, [SDV.IMM]Life Sciences [q-bio]/Immunology, TVM cells, TIM cells, [SDV.BC] Life Sciences [q-bio]/Cellular Biology
Abstract

International audience; The presence of CD8+ T cells with a memory phenotype in nonimmunized mice has been noted for decades, but it was not until about 2 decades ago that they began to be studied in greater depth. Currently called virtual memory CD8+ T cells, they consist of a heterogeneous group of cells with memory characteristics, without any previous contact with their specific antigens. These cells were identified in mice, but a few years ago, a cell type with characteristics equivalent to the murine ones was described in healthy humans. In this review, we address the different aspects of its biology mainly developed in murine models and what is currently known about its cellular equivalent in humans.

Published
2022

2. Anti-Glucosylsphingosine Autoimmunity, JAK2V617F-Dependent Interleukin-1β and JAK2V617F-Independent Cytokines in Myeloproliferative Neoplasms

Author

Edith Bigot-Corbel, Cédric Cleyrat, Eun Ho Eunice Choi, Laura Dufeu, Jean-Marc Gombert, François Girodon, Sophie Allain-Maillet, Nicolas Mennesson, Adrien Bosseboeuf, Yannick Le Bris, Olivier Mansier, Eric Lippert, Magali Pettazzoni, Sylvie Hermouet, Mégane Bostoën, Molecular Mechanisms of Chronic Inflammation in Hematological Diseases (CRCINA-ÉQUIPE 16), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), The University of New Mexico [Albuquerque], Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Hématologie [CHU Bordeaux], CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin, CHRU Brest - Service d'Hématologie (CHU-Brest-Hemato), Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Génétique, génomique fonctionnelle et biotechnologies (UMR 1078) (GGB), Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO)-Université de Brest (UBO)-EFS-Institut National de la Santé et de la Recherche Médicale (INSERM), Regulation of Bcl2 and p53 Networks in Multiple Myeloma and Mantle Cell Lymphoma (CRCINA-ÉQUIPE 10), Service d'Hématologie [Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), Laboratoire d'immunologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Service d'Hématologie Clinique (CHU de Dijon), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Lipides - Nutrition - Cancer [Dijon - U1231] (LNC), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Biochimie et Biologie Moléculaire Grand Est [HCL, Lyon] (Centre de Biologie et de Pathologie), Hospices Civils de Lyon (HCL), Laboratoire de Biochimie [Nantes], Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), EFS-Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, and Bernardo, Elizabeth

Subjects
0301 basic medicine, Cancer Research, IL-1Rα, medicine.medical_treatment, Clone (cell biology), interleukin-1β (IL-1β), Inflammation, [SDV.CAN]Life Sciences [q-bio]/Cancer, myeloproliferative neoplasms (MPNs), CALR exon 9 mutants, IP-10, medicine.disease_cause, lcsh:RC254-282, leptin, Article, Autoimmunity, Proinflammatory cytokine, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, Polycythemia vera, JAK2V617F, [SDV.CAN] Life Sciences [q-bio]/Cancer, glucolipids, hemic and lymphatic diseases, medicine, article clinique, auto-immunity, antigenic stimulation, business.industry, CRISPR technology, UT-7, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, glucosylsphingosine (GlcSph), cytokines, 3. Good health, Interleukin 33, 030104 developmental biology, Cytokine, Oncology, inflammation, 030220 oncology & carcinogenesis, Immunology, IL-33, medicine.symptom, business
Abstract

Inflammatory cytokines play a major role in myeloproliferative neoplasms (MPNs) as regulators of the MPN clone and as mediators of clinical symptoms and complications. Firstly, we investigated the effect of JAK2V617F on 42 molecules linked to inflammation. For JAK2V617F-mutated patients, the JAK2V617F allele burden (%JAK2V617F) correlated with the levels of IL-1&beta, IL-1R&alpha, IP-10 and leptin in polycythemia vera (PV), and with IL-33 in ET, for all other molecules, no correlation was found. Cytokine production was also studied in the human megakaryocytic cell line UT-7. Wild-type UT-7 cells secreted 27/42 cytokines measured. UT-7 clones expressing 50% or 75% JAK2V617F were generated, in which the production of IL-1&beta, IP-10 and RANTES was increased, other cytokines were not affected. Secondly, we searched for causes of chronic inflammation in MPNs other than driver mutations. Since antigen-driven selection is increasingly implicated in the pathogenesis of blood malignancies, we investigated whether proinflammatory glucosylsphingosine (GlcSph) may play a role in MPNs. We report that 20% (15/75) of MPN patients presented with anti-GlcSph IgGs, distinguished by elevated levels of 11 cytokines. In summary, only IL-1&beta, and IP-10 were linked to JAK2V617F both in patients and in UT-7 cells, other inflammation-linked cytokines in excess in MPNs were not. For subsets of MPN patients, a possible cause of inflammation may be auto-immunity against glucolipids.

Published
2020

3. Interleukin-1 Family Cytokines: Keystones in Liver Inflammatory Diseases

Author

Louise Barbier, Maroua Ferhat, Ephrem Salamé, Aurélie Robin, André Herbelin, Jean-Marc Gombert, Christine Silvain, Alice Barbarin, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Laboratoire d'immunologie [CHU Poitiers], Department of Hepatology and Gastroenterology, CHU de Poitiers, This study was supported by INSERM, CHU de Poitiers, Université de Poitiers, Ligue contre le Cancer (Comités départementaux de la Vienne, de la Charente, de la Charente Maritime et des Deux-Sèvres), and the Association pour la Recherche en Immunologie-Poitou-Charentes (ARIM-PC). MF and AB were supported by fellowships provided by INSERM, Région Poitou-Charentes, Octapharma, Fondation BrystolMeyers Squibb, and Région Nouvelle Aquitaine, respectively., and Barbarin, Alice

Subjects
0301 basic medicine, lcsh:Immunologic diseases. Allergy, [SDV.IMM] Life Sciences [q-bio]/Immunology, liver diseases, medicine.medical_treatment, Immunology, innate lymphoid cells, Inflammation, Review, Liver transplantation, Natural killer cell, Hepatitis, 03 medical and health sciences, trained immunity, 0302 clinical medicine, Immunity, invariant natural killer T-cells, medicine, Immunology and Allergy, Animals, Humans, Genetic Predisposition to Disease, innate immunity, Innate immune system, natural killer cells, business.industry, Innate lymphoid cell, Interleukin, Receptors, Interleukin-1, 3. Good health, Interleukin 33, 030104 developmental biology, medicine.anatomical_structure, inflammation, Multigene Family, interleukin-1 family cytokines, Cytokines, [SDV.IMM]Life Sciences [q-bio]/Immunology, Disease Susceptibility, medicine.symptom, business, lcsh:RC581-607, 030215 immunology, Interleukin-1
Abstract

International audience; The pyrogenic property being the first activity described, members of the interleukin-1 superfamily (IL-1α, IL-1β, IL-18, and the newest members: IL-33, IL-36, IL-37, and IL-38) are now known to be involved in several inflammatory diseases such as obesity, atherosclerosis, cancer, viral and parasite infections, and auto-inflammatory syndromes as well as liver diseases. Inflammation processes are keystones of chronic liver diseases, of which the etiology may be viral or toxic, as in alcoholic or non-alcoholic liver diseases. Inflammation is also at stake in acute liver failure involving massive necrosis, and in ischemia-reperfusion injury in the setting of liver transplantation. The role of the IL-1 superfamily of cytokines and receptors in liver diseases can be either protective or pro-inflammatory, depending on timing and the environment. Our review provides an overview of current understanding of the IL-1 family members in liver inflammation, highlighting recent key investigations, and therapeutic perspectives. We have tried to apply the concept of trained immunity to liver diseases, based on the role of the members of the IL-1 superfamily, first of all IL-1β but also IL-18 and IL-33, in modulating innate lymphoid immunity carried by natural killer cells, innate lymphoid cells or innate T-αβ lymphocytes.

Published
2019

4. Sustained treatment‐free remission in chronic myeloid leukaemia is associated with an increased frequency of innate CD8(+) T‐cells

Author

Alice Barbarin, Jean-Claude Chomel, Nathalie Piccirilli, François Guilhot, Xavier Leleu, Lydia Roy, Jean-Marc Gombert, Emilie Cayssials, Florence Jacomet, André Herbelin, Lucie Lefèvre, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Département d'Hématologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Laboratoire d'immunologie [CHU Poitiers], Hôpital Henri Mondor, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CIC - Poitiers, Université de Poitiers-Centre hospitalier universitaire de Poitiers (CHU Poitiers)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU de Poitiers-Service d’Oncologie Hématologique de Thérapie Cellulaire, Barbarin, Alice, and Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)

Subjects
Male, [SDV.IMM] Life Sciences [q-bio]/Immunology, Remission, Spontaneous, [SDV.CAN]Life Sciences [q-bio]/Cancer, CD8-Positive T-Lymphocytes, Positive correlation, Chronic myeloid leukaemia, 03 medical and health sciences, 0302 clinical medicine, [SDV.CAN] Life Sciences [q-bio]/Cancer, T-Lymphocyte Subsets, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Cytotoxic T cell, Medicine, Humans, Lymphocyte Count, Protein Kinase Inhibitors, ComputingMilieux_MISCELLANEOUS, business.industry, Hematology, Middle Aged, Control subjects, Immunity, Innate, 3. Good health, Killer Cells, Natural, 030220 oncology & carcinogenesis, Case-Control Studies, Immunology, Biomarker (medicine), [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, business, Tyrosine kinase, CD8, 030215 immunology
Abstract

Immunological mechanisms of treatment-free remission (TFR) in chronic myeloid leukaemia (CML) are poorly defined and, to date, no correlation between successful TFR and CD8(+) T-cell subsets has been found. We analysed a new identified human subset of CD8(+) T-cells, namely innate CD8(+) T-cells, in CML patients with TFR ≥ 2 years. We demonstrated a dramatic increase of functionally active innate CD8(+) T-cells in these patients as compared to control subjects and patients in remission under tyrosine kinase inhibitors. Moreover, we found a positive correlation between frequencies of innate CD8(+) T-cells and natural killer cells, possibly representing a new innate biomarker profile of successful TFR.

Published
2019

5. [The CD8+ T cell innate function in the war against cancer]

Author

Jean-Marc Gombert, Alice Barbarin, André Herbelin, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Poitiers, Laboratoire d'immunologie [CHU Poitiers], and Centre hospitalier universitaire de Poitiers (CHU Poitiers)

Subjects
0301 basic medicine, business.industry, Cancer, [SDV.CAN]Life Sciences [q-bio]/Cancer, General Medicine, Biology, medicine.disease, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 030104 developmental biology, Text mining, medicine, Cancer research, [SDV.IMM]Life Sciences [q-bio]/Immunology, Cytotoxic T cell, business, ComputingMilieux_MISCELLANEOUS, Function (biology)
Abstract

International audience; no abstract

Published
2017

6. The Impact of Invariant NKT Cells in Sterile Inflammation: The Possible Contribution of the Alarmin/Cytokine IL-33

Author

Maroua Haroun Ferhat, Aurélie Robin, Louise Barbier, Antoine Thierry, Jean-Marc Gombert, Alice Barbarin, André Herbelin, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre hospitalier universitaire de Poitiers (CHU Poitiers), Departement d'Hépato-Gastroentérologie et Cancérologie Digestive [CHRU Tours], Centre Hospitalier Régional Universitaire de Tours (CHRU TOURS), Laboratoire d'immunologie [CHU Poitiers], Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), and Barbarin, Alice

Subjects
0301 basic medicine, lcsh:Immunologic diseases. Allergy, sterile inflammatory response, [SDV.IMM] Life Sciences [q-bio]/Immunology, medicine.medical_treatment, Sterile inflammation, Immunology, Endogeny, Biology, 03 medical and health sciences, 0302 clinical medicine, Immune system, medicine, alarmin IL-33, ischemia reperfusion, Immunology and Allergy, Alarmins, Animals, Humans, tissue repair, Nuclear protein, Inflammation, Natural killer T cell, Interleukin-33, Pathophysiology, 3. Good health, CD1d-restricted T cells, Interleukin 33, 030104 developmental biology, Cytokine, iNKT, Perspective, Cytokines, Natural Killer T-Cells, [SDV.IMM]Life Sciences [q-bio]/Immunology, lcsh:RC581-607, Biomarkers, 030215 immunology
Abstract

International audience; Although the contribution of iNKT cells to induction of sterile inflammation is now well-established, the nature of the endogenous compounds released early after cellular stress or damage that drive their activation and recruitment remains poorly understood. More precisely, iNKT cells have not been described as being reactive to endogenous non-protein damage-associated molecular-pattern molecules (DAMPs). A second subset of DAMPs, called alarmins, are tissue-derived nuclear proteins, constitutively expressed at high levels in epithelial barrier tissues and endothelial barriers. These potent immunostimulants, immediately released after tissue damage, include the alarmin IL-33. This factor has aroused interest due to its singular action as an alarmin during infectious, allergic responses and acute tissue injury, and as a cytokine, contributing to the latter resolutive/repair phase of sterile inflammation. IL-33 targets iNKT cells, inducing their recruitment in an inflammatory state, and amplifying their regulatory and effector functions. In the present review, we introduce the new concept of a biological axis of iNKT cells and IL-33, involved in alerting and controlling the immune cells in experimental models of sterile inflammation. This review will focus on acute organ injury models, especially ischemia-reperfusion injury, in the kidneys, liver and lungs, where iNKT cells and IL-33 have been presumed to mediate and/or control the injury mechanisms, and their potential relevance in human pathophysiology.

Published
2018

7. [The CD8+ T cell innate function in the war against cancer]

Author

Barbarin, Alice, Herbelin, André, Gombert, Jean-Marc, Barbarin, Alice, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'immunologie [CHU Poitiers], and Centre hospitalier universitaire de Poitiers (CHU Poitiers)

Subjects
[SDV.IMM] Life Sciences [q-bio]/Immunology, [SDV.CAN] Life Sciences [q-bio]/Cancer, [SDV.IMM]Life Sciences [q-bio]/Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, ComputingMilieux_MISCELLANEOUS
Abstract

International audience; no abstract

Published
2017

8. The Rho- ROCK pathway as a new pathological mechanism of innate immune subversion in chronic myeloid leukaemia

Author

Basbous, Sara, Levescot, Anaïs, Piccirilli, Nathalie, Brizard, Françoise, Guilhot, François, Roy, Lydia, Bourmeyster, Nicolas, Gombert, Jean-Marc, Herbelin, André, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre hospitalier universitaire de Poitiers (CHU Poitiers), CIC - Poitiers, Université de Poitiers-Centre hospitalier universitaire de Poitiers (CHU Poitiers)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Henri Mondor, Institut de Physiologie et Biologie Cellulaires (IPBC), Université de Poitiers-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'immunologie [CHU Poitiers], Centre National de la Recherche Scientifique (CNRS)-Université de Poitiers, and Barbarin, Alice

Subjects
[SDV.IMM] Life Sciences [q-bio]/Immunology, [SDV.CAN] Life Sciences [q-bio]/Cancer, [SDV.IMM]Life Sciences [q-bio]/Immunology, [SDV.CAN]Life Sciences [q-bio]/Cancer, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2016

9. Evidence for eomesodermin-expressing innate-like CD8 + KIR/NKG2A + T cells in human adults and cord blood samples

Author

Jacomet, Florence, Cayssials, Emilie, Basbous, Sara, Levescot, Anaïs, Piccirilli, Nathalie, Desmier, Déborah, Robin, Aurélie, Barra, Anne, Giraud, Christine, Guilhot, François, Roy, Lydia, Herbelin, André, Gombert, Jean-Marc, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'immunologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Etablissement français du sang [Poitiers] (EFS), CIC - Poitiers, Université de Poitiers-Centre hospitalier universitaire de Poitiers (CHU Poitiers)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Henri Mondor, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Poitiers, and Barbarin, Alice

Subjects
[SDV.IMM] Life Sciences [q-bio]/Immunology, [SDV.IMM]Life Sciences [q-bio]/Immunology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2015

10. Strategies to model AL amyloidosis in mice

Author

Corinne Lacombe, Arnaud Jaccard, Michel Cogné, Guy Touchard, Sébastien Bender, Christophe Sirac, Franck Bridoux, Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations (PMRIL), Université de Limoges (UNILIM)-Génomique, Environnement, Immunité, Santé, Thérapeutique (GEIST FR CNRS 3503)-Centre National de la Recherche Scientifique (CNRS), Service d'Hématologie clinique et thérapie cellulaire [CHU Limoges], CHU Limoges, Service de néphrologie - hémodialyse et transplantation rénale, Centre hospitalier universitaire de Poitiers (CHU Poitiers), and Laboratoire d'immunologie [CHU Poitiers]

Subjects
MESH: DNA Primers, NLM, Transgene, Lymphoproliferative disorders, Disease, MESH: Base Sequence, Biology, Immunoglobulin light chain, Polymerase Chain Reaction, Mass Spectrometry, law.invention, Mice, 03 medical and health sciences, 0302 clinical medicine, law, Internal Medicine, medicine, AL amyloidosis, Animals, MESH: Amyloidosis, MESH: Animals, MESH: Mice, Severe complication, Polymerase chain reaction, DNA Primers, 030304 developmental biology, MESH: Mass Spectrometry, 0303 health sciences, Base Sequence, [CHIM.ORGA]Chemical Sciences/Organic chemistry, MESH: Polymerase Chain Reaction, Amyloidosis, medicine.disease, 3. Good health, Transgenesis, Disease Models, Animal, 030220 oncology & carcinogenesis, Immunology, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Disease Models, Animal
Abstract

International audience; Monoclonal immunoglobulin (Ig) deposition in AL amyloidosis is a severe complication of lymphoproliferative disorders. Research on this disease suffers from the lack of animal models, as they could allow for the testing of new innovative therapeutic strategies. We are trying to develop a transgenic animal model for this disease by overexpressing Ig light chain (LC) sequences cloned from AL amyloidosis patients. After several unsuccessful attempts using additional transgenesis due to low LC expression, we currently are following a strategy of targeted insertion of human LC sequences in the mouse endogenous kappa LC locus. We describe here the first data from this ‘knock-in’ model and propose future prospects to increase the rates of free LC and mimic the human disease. Absence of amyloid deposits in such models would raise the possibility of a resistance to AL amyloidosis in mice and question the feasibility of a reliable animal model for this disease.

Published
2011
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11. The Alarmin Concept Applied to Human Renal Transplantation: Evidence for a Differential Implication of HMGB1 and IL-33

Author

Jean-Philippe Girard, Guy Touchard, Antoine Thierry, Sébastien Giraud, Thierry Hauet, Aurélie Robin, Virginie Ameteau, Anne Barra, Franck Bridoux, André Herbelin, Jean-Marc Gombert, Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques ( IRTOMIT), Université de Poitiers-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'immunologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Service de néphrologie - hémodialyse et transplantation rénale, Institut de pharmacologie et de biologie structurale (IPBS), Université Toulouse III - Paul Sabatier (UT3), 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 Toulouse III - Paul Sabatier (UT3), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées

Subjects
[SDV]Life Sciences [q-bio], lcsh:Medicine, Umbilical vein, Cohort Studies, 0302 clinical medicine, Molecular Cell Biology, Renal Transplantation, Prospective Studies, HMGB1 Protein, lcsh:Science, Kidney transplantation, ComputingMilieux_MISCELLANEOUS, Cellular Stress Responses, White Cells, 0303 health sciences, Kidney, Multidisciplinary, biology, Hematology, Middle Aged, Flow Cytometry, Cell Hypoxia, Innate Immunity, medicine.anatomical_structure, Transplant Surgery, Nephrology, Reperfusion Injury, Medicine, Research Article, Adult, medicine.medical_specialty, Urinary system, Enzyme-Linked Immunosorbent Assay, chemical and pharmacologic phenomena, Real-Time Polymerase Chain Reaction, HMGB1, Statistics, Nonparametric, 03 medical and health sciences, Internal medicine, Human Umbilical Vein Endothelial Cells, medicine, Humans, Immunoassays, Biology, Aged, 030304 developmental biology, Transplantation, business.industry, Interleukins, lcsh:R, Immunity, Immunologic Subspecialties, Interleukin-33, medicine.disease, Kidney Transplantation, Immunity, Innate, TLR2, Endocrinology, Immunology, Immunologic Techniques, biology.protein, lcsh:Q, Clinical Immunology, Surgery, business, Reperfusion injury, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, 030215 immunology
Abstract

The endogenous molecules high mobility group box 1 (HMGB1) and interleukin-33 (IL-33) have been identified as alarmins, capable of mediating danger signals during tissue damage. Here, we address their possible role as innate-immune mediators in ischemia-reperfusion injury (IRI) following human kidney transplantation. We analysed serum and urinary HMGB1 and IL-33 levels, all determined by enzyme-linked immunosorbent assay, in a cohort of 26 deceased renal transplant recipients. Urinary HMGB1 and IL-33 levels were significantly increased as soon as 30 min after reperfusion, as compared to those before treatment. Moreover, both serum and urinary IL-33 (but not HMGB1) increase was positively correlated with cold ischemia time, from 30 min to 3 days post-transplantation. In vitro, human umbilical vein endothelial cells subjected to hypoxia conditions released both HMGB-1 and IL-33, while only the latter was further increased upon subsequent re-oxygenation. Finally, we postulate that leukocytes from renal recipient patients are targeted by both HMGB1 and IL-33, as suggested by increased transcription of their respective receptors (TLR2/4 and ST2L) shortly after transplantation. Consistent with this view, we found that iNKT cells, an innate-like T cell subset involved in IRI and targeted by IL-33 but not by HMGB1 was activated 1 hour post-transplantation. Altogether, these results are in keeping with a potential role of IL-33 as an innate-immune mediator during kidney IRI in humans.

Published
2014

12. The pro-Th2 cytokine IL-33 directly interacts with invariant NKT and NK cells to induce IFN-gamma production

Author

Michel Samson, Elvire Bourgeois, Pierre Gourdy, Séverine Diem, Stéphane Roga, Elke Schneider, Michel Dy, Linh Pham Van, Jean-Philippe Girard, Anne Barra, André Herbelin, Jean-Marc Gombert, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Détoxication et réparation tissulaire, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), Laboratoire d'immunologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Institut de pharmacologie et de biologie structurale (IPBS), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), CNRS, Université de Paris Descartes, Ligue Nationale contre le Cancer, la Chancellerie des Universités de Paris, Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140, Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Slama, Catherine, Université de Rennes (UR), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cytokines, hématopoïèse et réponse immune ( CHRI ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Signalisation et Réponses aux Agents Infectieux et Chimiques ( SeRAIC ), Université de Rennes 1 ( UR1 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -IFR140, Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -IFR140-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre hospitalier universitaire de Poitiers ( CHU Poitiers ), Institut de pharmacologie et de biologie structurale ( IPBS ), Centre National de la Recherche Scientifique ( CNRS ) -Université Toulouse III - Paul Sabatier ( UPS ), Institut des Maladies Métaboliques et Cardiovasculaires ( I2MC ), Université Toulouse III - Paul Sabatier ( UPS ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Hôpital de Rangueil, CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de médecine moléculaire de Rangueil ( I2MR ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Paris Descartes - Paris 5 ( UPD5 ), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM), 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)

Subjects
MESH: Interleukin-12, MESH: Spleen, medicine.medical_treatment, MESH: Mice, Knockout, Interleukin 21, Mice, 0302 clinical medicine, Immunology and Allergy, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH : Female, MESH: Animals, IL-2 receptor, ComputingMilieux_MISCELLANEOUS, Mice, Knockout, 0303 health sciences, Mice, Inbred BALB C, ZAP70, Natural killer T cell, Interleukin-12, Killer Cells, Natural, Cytokine, Liver, Interleukin 12, Cytokines, Natural killer cells, Natural killer T cells, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, MESH : Killer Cells, Natural, MESH : Spleen, MESH: Killer Cells, Natural, MESH: Interleukins, MESH: Interferon-gamma, Immunology, MESH: Mice, Inbred BALB C, MESH : Mice, Inbred C57BL, Biology, MESH : Interleukin-4, 03 medical and health sciences, Interferon-gamma, Th2 Cells, MESH: Mice, Inbred C57BL, MESH: Th2 Cells, MESH : Mice, medicine, MESH : Interleukin-12, Animals, Humans, MESH: Mice, MESH : Mice, Inbred BALB C, MESH : Interferon-gamma, 030304 developmental biology, Inflammation, Lymphokine-activated killer cell, MESH: Humans, Interleukins, MESH : Humans, MESH : Liver, MESH: Interleukin-4, Interleukin-33, MESH : Natural Killer T-Cells, MESH : Th2 Cells, Interleukin 33, Mice, Inbred C57BL, MESH: Natural Killer T-Cells, Natural Killer T-Cells, MESH : Mice, Knockout, Th1/Th2 cells, Interleukin-4, MESH : Animals, MESH : Interleukins, MESH: Female, Spleen, 030215 immunology, MESH: Liver
Abstract

International audience; IL-33 has recently been identified as a cytokine endowed with pro-Th2 functions, raising the question of its effect on invariant natural killer T cell (iNKT), which are potent IL-4 producers. Here, we report a two-fold increase of iNKT-cell counts in spleen and liver after a 7-day treatment of mice with IL-33, which results from a direct effect, given that purified iNKT cells express the T1/ST2 receptor constitutively and respond to IL-33 by in vitro expansion and functional activation. Conversely to the expected pro-Th2 effect, IL-33 induced a preferential increase in IFN-gamma rather than IL-4 production upon TCR engagement that depended on endogenous IL-12. Moreover, in combination with the pro-inflammatory cytokine IL-12, IL-33 enhanced IFN-gamma production by both iNKT and NK cells. Taken together these data support the conclusion that IL-33 can contribute as a co-stimulatory factor to innate cellular immune responses.

Published
2009

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