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5 results on '"APPEL À PROJETS GÉNÉRIQUE 2018 - Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome. - - NASHILCCD82018 - ANR-18-CE15-0024 - AAPG2018 - VALID"'

1. Synergistic prostaglandin E synthesis by myeloid and endothelial cells promotes fetal hematopoietic stem cell expansion in vertebrates

Author

Pietro Cacialli, Marie‐Pierre Mailhe, Ingrid Wagner, Doron Merkler, Rachel Golub, Julien Y Bertrand, Université de Genève = University of Geneva (UNIGE), Lymphocytes et Immunité - Lymphocytes and Immunity, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), RG work is supported by Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Université de Paris, and ANR project NASHILCCD8 (#18-CE15-0024-01). JYB is funded by the Swiss National Fund (310030_184814). DM is funded by the Swiss National Fund (310030B_201271). Open access funding provided by Universite de Geneve., ANR-18-CE15-0024,NASHILCCD8,Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome.(2018), Vougny, Marie-Christine, APPEL À PROJETS GÉNÉRIQUE 2018 - Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome. - - NASHILCCD82018 - ANR-18-CE15-0024 - AAPG2018 - VALID, Cacialli P., Mailhe M.-P., Wagner I., Merkler D., Golub R., and Bertrand J.Y.

Subjects
General Immunology and Microbiology, [SDV.IMM] Life Sciences [q-bio]/Immunology, slco2b1, Animal, Hemangioblasts, General Neuroscience, Hematopoietic Stem Cell, HSC, Hemangioblast, Hematopoietic Stem Cells, General Biochemistry, Genetics and Molecular Biology, Dinoprostone, Mice, hematopoietic niche, HSCs, Animals, Prostaglandin H2, [SDV.IMM]Life Sciences [q-bio]/Immunology, PGE2, Molecular Biology, Zebrafish
Abstract

International audience; During development, hematopoietic stem cells (HSCs) are produced from the hemogenic endothelium and will expand in a transient hematopoietic niche. Prostaglandin E2 (PGE2) is essential during vertebrate development and HSC specification, but its precise source in the embryo remains elusive. Here, we show that in the zebrafish embryo, PGE2 synthesis genes are expressed by distinct stromal cell populations, myeloid (neutrophils, macrophages), and endothelial cells of the caudal hematopoietic tissue. Ablation of myeloid cells, which produce the PGE2 precursor prostaglandin H2 (PGH2), results in loss of HSCs in the caudal hematopoietic tissue, which could be rescued by exogeneous PGE2 or PGH2 supplementation. Endothelial cells contribute by expressing the PGH2 import transporter slco2b1 and ptges3, the enzyme converting PGH2 into PGE2. Of note, differential niche cell expression of PGE2 biosynthesis enzymes is also observed in the mouse fetal liver. Taken altogether, our data suggest that the triad composed of neutrophils, macrophages, and endothelial cells sequentially and synergistically contributes to blood stem cell expansion during vertebrate development.

Published
2022

2. Signaling Pathways Tuning Innate Lymphoid Cell Response to Hepatocellular Carcinoma

Author

Bourayou, Elsa, Golub, Rachel, Lymphocytes et Immunité - Lymphocytes and Immunity, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), This work has been supported by Institut Pasteur, Université de Paris, Institut National de la santé et de la recherche Médicale (INSERM) and by grants from the French Government (National Research Agency, ANR), ANR project NASHILCCD8 (#18-CE15-0024-01)., ANR-18-CE15-0024,NASHILCCD8,Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome.(2018), Vougny, Marie-Christine, and APPEL À PROJETS GÉNÉRIQUE 2018 - Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome. - - NASHILCCD82018 - ANR-18-CE15-0024 - AAPG2018 - VALID

Subjects
Carcinoma, Hepatocellular, [SDV.IMM] Life Sciences [q-bio]/Immunology, Notch and TGF-β pathways, Immunology, Liver Neoplasms, NASH, NK cells, liver, Immunity, Innate, digestive system diseases, ILC1, Killer Cells, Natural, inflammation, Immunology and Allergy, Humans, [SDV.IMM]Life Sciences [q-bio]/Immunology, HCC, Signal Transduction
Abstract

International audience; Hepatocellular carcinoma (HCC) is one of the deadliest cancers worldwide and its incidence continues to rise globally. Various causes can lead to its development such as chronic viral infections causing hepatitis, cirrhosis or nonalcoholic steatohepatitis (NASH). The contribution of immune cells to HCC development and progression has been extensively studied when it comes to adaptive lymphocytes or myeloid populations. However, the role of the innate lymphoid cells (ILCs) is still not well defined. ILCs are a family of lymphocytes comprising five subsets including circulating Natural Killer (NK) cells, ILC1s, ILC2s, ILC3s and lymphocytes tissue-inducer cells (LTi). Mostly located at epithelial surfaces, tissue-resident ILCs and NK cells can rapidly react to environmental changes to mount appropriate immune responses. Here, we provide an overview of their roles and actions in HCC with an emphasis on the importance of diverse signaling pathways (Notch, TGF-β, Wnt/β-catenin…) in the tuning of their response to HCC.

Published
2022

3. The Notch signaling pathway involvement in innate lymphoid cell biology

Author

Rachel Golub, Lymphocytes et Immunité - Lymphocytes and Immunity, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), RG work is supported by Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Université de Paris, and ANR project NASHILCCD8(#18-CE15-0024-01), Projets ARC 2020 PJA3, Fonds AMGENFrance., ANR-18-CE15-0024,NASHILCCD8,Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome.(2018), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Lassailly-Bondaz, Anne, and APPEL À PROJETS GÉNÉRIQUE 2018 - Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome. - - NASHILCCD82018 - ANR-18-CE15-0024 - AAPG2018 - VALID

Subjects
0301 basic medicine, Medicine (General), [SDV.IMM] Life Sciences [q-bio]/Immunology, QH301-705.5, Notch pathway, Notch signaling pathway, Stimulation, Biology, Cell fate determination, 03 medical and health sciences, 0302 clinical medicine, Immune system, R5-920, Secretion, Lymphocytes, Biology (General), skin and connective tissue diseases, Development of lymphoid cells, Innate lymphoid cell, Cell Differentiation, General Medicine, Immunity, Innate, Cell biology, Immune functions, body regions, 030104 developmental biology, ILC, Review Article: Special Edition, 030220 oncology & carcinogenesis, [SDV.IMM]Life Sciences [q-bio]/Immunology, Polarization of immune subsets, Signal Transduction
Abstract

International audience; The role of Notch in the immune system was first described in the late 90s. Reports revealed that Notch is one of the most conserved developmental pathways involved in diverse biological processes such as the development, differentiation, survival and functions of many immune populations. Here, we provide an extended view of the pleiotropic effects of the Notch signaling on the innate lymphoid cell (ILC) biology. We review the current knowledge on Notch signaling in the regulation of ILC differentiation, plasticity and functions in diverse tissue types and at both the fetal and adult developmental stages. ILCs are early responder cells that secrete a large panel of cytokines after stimulation. By controlling the abundance of ILCs and the specificity of their release, the Notch pathway is also implicated in the regulation of their functions. The Notch pathway is therefore an important player in both ILC cell fate decision and ILC immune response.

Published
2021

4. The interplay between innate lymphoid cells and T cells

Author

Gayetri Ramachandran, Rachel Golub, Marie Cherrier, Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Lymphocytes et Immunité - Lymphocytes and Immunity, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), M.C. is supported by INSERM and Association François Aupetit dedicated to patients suffering from IBD. R.G. work is supported by Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Université de Paris, and ANR project NASHILCCD8 (#18-CE15-0024-01)., We thank Serge van de Pavert for critical discussions and for review of the paper., ANR-18-CE15-0024,NASHILCCD8,Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome.(2018), Vougny, Marie-Christine, APPEL À PROJETS GÉNÉRIQUE 2018 - Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome. - - NASHILCCD82018 - ANR-18-CE15-0024 - AAPG2018 - VALID, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), and Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)

Subjects
0301 basic medicine, Cell type, [SDV.IMM] Life Sciences [q-bio]/Immunology, Immunology, Context (language use), Cell Communication, Biology, Gut flora, Adaptive Immunity, Lymphocyte Activation, Substrate Specificity, Immunomodulation, 03 medical and health sciences, 0302 clinical medicine, Immune system, T-Lymphocyte Subsets, Immunology and Allergy, Animals, Humans, skin and connective tissue diseases, Immunity, Cellular, Innate lymphoid cell, Cell Differentiation, Acquired immune system, biology.organism_classification, Immunity, Innate, body regions, 030104 developmental biology, Gene Expression Regulation, Host-Pathogen Interactions, [SDV.IMM]Life Sciences [q-bio]/Immunology, Neuroscience, Immunologic Memory, Function (biology), Homeostasis, Biomarkers, 030215 immunology, Signal Transduction
Abstract

International audience; ILCs and T cells are closely related functionally but they significantly differ in their ability to circulate, expand, and renew. Cooperation and reciprocal functional regulation suggest that these cell types are more complementary than simply redundant during immune responses. How ILCs shape T-cell responses is strongly dependent on the tissue and inflammatory context. Likewise, indirect regulation of ILCs by adaptive immunity is induced by environmental cues such as the gut microbiota. Here, we review shared requirements for the development and function of both cell types and divergences in the orchestration of prototypic immune functions. We discuss the diversity of functional interactions between T cells and ILCs during homeostasis and immune responses. Identifying the location and the nature of the tissue microenvironment in which these interactions are taking place may uncover the remaining mysteries of their close encounters.

Published
2020

5. Natural Killer Cells and Type 1 Innate Lymphoid Cells Are New Actors in Non-alcoholic Fatty Liver Disease

Author

Rachel Golub, Philippe Gual, Elodie Vieira, Carmelo Luci, Thibaut Perchet, Vougny, Marie-Christine, INTERACTION ENTRE ALCOOL ET L'OBÉSITÉ DANS LA SÉVÉRITÉ DES MALADIES DU FOIE GRAS. - - HEPAMETOL2015 - ANR-15-CE14-0016 - AAPG2015 - VALID, APPEL À PROJETS GÉNÉRIQUE 2018 - Etude de la signalisation SYK dans les maladies inflammatoires chroniques - - INFLAMMASYK2018 - ANR-18-CE14-0019 - AAPG2018 - VALID, Centres d'excellences - Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie - - SIGNALIFE2011 - ANR-11-LABX-0028 - LABX - VALID, APPEL À PROJETS GÉNÉRIQUE 2018 - Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome. - - NASHILCCD82018 - ANR-18-CE15-0024 - AAPG2018 - VALID, Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Lymphopoïèse (Lymphopoïèse (UMR_1223 / U1223 / U-Pasteur_4)), Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), This work is supported by grants from Institut National de la santé et de la recherche Médicale (INSERM), Université Côte d'Azur and charities (Association Française pour l'Etude du Foie (AFEF)/LFB to PG). This work was also funded by the French Government (National Research Agency, ANR): #ANR-15-CE14-0016-01, #ANR-18-CE14-0019-02 and through the Investments for the Future LABEX SIGNALIFE (#ANR-11-LABX-0028-01) and the UCAJEDI Investments in the Future project (#ANR-15-IDEX-01). This work was supported by the Fondation pour la Recherche Médicale, grant number ECO20170637473 to EV, TP, and RG work is supported by Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Université Paris Diderot, and ANR project NASHILCCD8 (#18-CE15-0024-01)., ANR-15-CE14-0016,HEPAMETOL,INTERACTION ENTRE ALCOOL ET L'OBÉSITÉ DANS LA SÉVÉRITÉ DES MALADIES DU FOIE GRAS.(2015), ANR-18-CE14-0019,INFLAMMASYK,Etude de la signalisation SYK dans les maladies inflammatoires chroniques(2018), ANR-11-LABX-0028,SIGNALIFE,Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie(2011), ANR-18-CE15-0024,NASHILCCD8,Contribution des ILC et des cellules T CD8 à la stéatose hépatique non alcoolique et à sa progression vers l'hépatocarcinome.(2018), Université Nice Sophia Antipolis (... - 2019) (UNS), and Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
0301 basic medicine, lcsh:Immunologic diseases. Allergy, [SDV.IMM] Life Sciences [q-bio]/Immunology, Mini Review, Population, Immunology, Inflammation, NK cells, Biology, liver, ILC1, 03 medical and health sciences, 0302 clinical medicine, Immune system, Non-alcoholic Fatty Liver Disease, NAFLD, medicine, Immunology and Allergy, Animals, Humans, Lymphocytes, education, Liver injury, education.field_of_study, Fatty liver, Innate lymphoid cell, NASH, medicine.disease, Immunity, Innate, 3. Good health, Gastrointestinal Tract, Killer Cells, Natural, 030104 developmental biology, medicine.anatomical_structure, Adipose Tissue, inflammation, Hepatocyte, [SDV.IMM]Life Sciences [q-bio]/Immunology, medicine.symptom, Steatohepatitis, Energy Metabolism, lcsh:RC581-607, Biomarkers, 030215 immunology
Abstract

International audience; Obesity and associated liver diseases (Non Alcoholic Fatty Liver Disease, NAFLD) are a major public health problem with increasing incidence in Western countries (25% of the affected population). These complications develop from a fatty liver (steatosis) to an inflammatory state (steatohepatitis) evolving toward fibrosis and hepatocellular carcinoma. Lipid accumulation in the liver contributes to hepatocyte cell death and promotes liver injury. Local immune cells are activated either by Danger Associated Molecular Patterns (DAMPS) released by dead hepatocytes or by bacterial products (PAMPS) reaching the liver due to increased intestinal permeability. The resulting low-grade inflammatory state promotes the progression of liver complications toward more severe grades. Innate lymphoid cells (ILC) are an heterogeneous family of five subsets including circulating Natural Killer (NK) cells, ILC1, ILC2, ILC3, and lymphocytes tissue-inducer cells (LTi). NK cells and tissue-resident ILCs, mainly located at epithelial surfaces, are prompt to rapidly react to environmental changes to mount appropriate immune responses. Recent works have demonstrated the interplay between ILCs subsets and the environment within metabolic active organs such as liver, adipose tissue and gut during diet-induced obesity leading or not to hepatic abnormalities. Here, we provide an overview of the newly roles of NK cells and ILC1 in metabolism focusing on their contribution to the development of NAFLD. We also discuss recent studies that demonstrate the ability of these two subsets to influence tissue-specific metabolism and how their function and homeostasis are affected during metabolic disorders.

Published
2019

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