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Start Over Descriptor "innate lymphocyte" Topic immunity, innate
9 results on '"innate lymphocyte"'

1. Innate lymphocytes: pathogenesis and therapeutic targets of liver diseases and cancer.

Author

Chen Y and Tian Z

Subjects
Animals, Humans, Liver Diseases immunology, Liver Diseases therapy, Neoplasms immunology, Neoplasms therapy, Homeostasis, Immune Tolerance, Immunity, Innate, Killer Cells, Natural immunology, Liver Diseases pathology, Lymphocytes immunology, Neoplasms pathology
Abstract

The liver is a lymphoid organ with unique immunological properties, particularly, its predominant innate immune system. The balance between immune tolerance and immune activity is critical to liver physiological functions and is responsible for the sensitivity of this organ to numerous diseases, including hepatotropic virus infection, alcoholic liver disease, nonalcoholic fatty liver disease, autoimmune liver disease, and liver cancer, which are major health problems globally. In the past decade, with the discovery of liver-resident natural killer cells, the importance of innate lymphocytes with tissue residency has gradually become the focus of research. In this review, we address the current knowledge regarding hepatic innate lymphocytes with unique characteristics, including NK cells, ILC1/2/3s, NKT cells, γδ T cells, and MAIT cells, and their potential roles in liver homeostasis maintenance and the progression of liver diseases and cancer. A better understanding of the immunopathogenesis of hepatic innate lymphocytes will be helpful for proposing effective treatments for liver diseases and cancer.

Published
2021
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2. Human T-bet Governs Innate and Innate-like Adaptive IFN-γ Immunity against Mycobacteria.

Author

Yang R, Mele F, Worley L, Langlais D, Rosain J, Benhsaien I, Elarabi H, Croft CA, Doisne JM, Zhang P, Weisshaar M, Jarrossay D, Latorre D, Shen Y, Han J, Ogishi M, Gruber C, Markle J, Al Ali F, Rahman M, Khan T, Seeleuthner Y, Kerner G, Husquin LT, Maclsaac JL, Jeljeli M, Errami A, Ailal F, Kobor MS, Oleaga-Quintas C, Roynard M, Bourgey M, El Baghdadi J, Boisson-Dupuis S, Puel A, Batteux F, Rozenberg F, Marr N, Pan-Hammarström Q, Bogunovic D, Quintana-Murci L, Carroll T, Ma CS, Abel L, Bousfiha A, Di Santo JP, Glimcher LH, Gros P, Tangye SG, Sallusto F, Bustamante J, and Casanova JL

Subjects
Amino Acid Sequence, Base Sequence, Cell Lineage, Child, Preschool, Chromatin metabolism, CpG Islands genetics, DNA Methylation genetics, Dendritic Cells metabolism, Epigenesis, Genetic, Female, Homozygote, Humans, INDEL Mutation genetics, Infant, Interferon-gamma metabolism, Killer Cells, Natural cytology, Killer Cells, Natural metabolism, Loss of Function Mutation genetics, Male, Mycobacterium Infections genetics, Mycobacterium Infections immunology, Mycobacterium Infections microbiology, Pedigree, T-Box Domain Proteins chemistry, T-Box Domain Proteins deficiency, T-Box Domain Proteins genetics, T-Lymphocytes, Helper-Inducer immunology, Transcriptome genetics, Adaptive Immunity, Immunity, Innate, Interferon-gamma immunology, Mycobacterium immunology, T-Box Domain Proteins metabolism
Abstract

Inborn errors of human interferon gamma (IFN-γ) immunity underlie mycobacterial disease. We report a patient with mycobacterial disease due to inherited deficiency of the transcription factor T-bet. The patient has extremely low counts of circulating Mycobacterium-reactive natural killer (NK), invariant NKT (iNKT), mucosal-associated invariant T (MAIT), and Vδ2 + γδ T lymphocytes, and of Mycobacterium-non reactive classic T H 1 lymphocytes, with the residual populations of these cells also producing abnormally small amounts of IFN-γ. Other lymphocyte subsets develop normally but produce low levels of IFN-γ, with the exception of CD8 + αβ T and non-classic CD4 + αβ T H 1 ∗ lymphocytes, which produce IFN-γ normally in response to mycobacterial antigens. Human T-bet deficiency thus underlies mycobacterial disease by preventing the development of innate (NK) and innate-like adaptive lymphocytes (iNKT, MAIT, and Vδ2 + γδ T cells) and IFN-γ production by them, with mycobacterium-specific, IFN-γ-producing, purely adaptive CD8 + αβ T, and CD4 + αβ T H 1 ∗ cells unable to compensate for this deficit., Competing Interests: Declaration of Interests L.H.G. serves on the Board of Directors of GlaxoSmithKline Pharmaceutical Company and the Analog Device Corporation and formerly served on the Boards of Bristol Myers Squibb Pharmaceutical Company and the Waters Corporation. She is also on the Scientific Advisory Boards of Abpro, Kaleido, and Repare biotechnology companies. J.-L.C. serves on the Scientific Advisory Boards of ADMA Biologics Inc., Celgene, and Kymera Therapeutics, Inc. He also consults for Elixiron Immunotherapeutics. Other authors declare no competing interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Published
2020
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3. Group 2 Innate Lymphoid Cells (ILC2): Type 2 Immunity and Helminth Immunity.

Author

Herbert DR, Douglas B, and Zullo K

Subjects
Animals, Cell Lineage immunology, Helminthiasis parasitology, Helminths pathogenicity, Humans, Immunity, Innate genetics, Interleukin-13 genetics, Interleukin-5 genetics, Mice, Helminthiasis immunology, Helminths immunology, Immunity, Innate immunology, Lymphocytes immunology
Abstract

Group 2 innate lymphoid cells (ILC2) have emerged as a major component of type 2 inflammation in mice and humans. ILC2 secrete large amounts of interleukins 5 and 13, which are largely responsible for host protective immunity against helminth parasites because these cytokines induce profound changes in host physiology that include: goblet cell metaplasia, mucus accumulation, smooth muscle hypercontractility, eosinophil and mast cell recruitment, and alternative macrophage activation (M2). This review covers the initial recognition of ILC2 as a distinct cell lineage, the key studies that established their biological importance, particularly in helminth infection, and the new directions that are likely to be the focus of emerging work that further explores this unique cell population in the context of health and disease.

Published
2019
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4. Tissue-Resident Lymphocytes Across Innate and Adaptive Lineages.

Author

Chou C and Li MO

Subjects
Animals, Humans, Infections pathology, Lymphocytes pathology, Neoplasms pathology, Adaptive Immunity, Immunity, Innate, Infections immunology, Lymphocytes immunology, Neoplasms immunology
Abstract

Lymphocytes are an integral component of the immune system. Classically, all lymphocytes were thought to perpetually recirculate between secondary lymphoid organs and only traffic to non-lymphoid tissues upon activation. In recent years, a diverse family of non-circulating lymphocytes have been identified. These include innate lymphocytes, innate-like T cells and a subset of conventional T cells. Spanning the innate-adaptive spectrum, these tissue-resident lymphocytes carry out specialized functions and cross-talk with other immune cell types to maintain tissue integrity and homeostasis both at the steady state and during pathological conditions. In this review, we provide an overview of the heterogeneous tissue-resident lymphocyte populations, discuss their development, and highlight their functions both in the context of microbial infection and cancer.

Published
2018
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6. Human T-bet Governs Innate and Innate-like Adaptive IFN-γ Immunity against Mycobacteria

Author

Laurent Abel, Laurie H. Glimcher, Lluis Quintana-Murci, Nico Marr, Fatima Al Ali, Jean Marc Doisne, David Langlais, Jacinta Bustamante, Marc Weisshaar, Jing Han, Jamila El Baghdadi, Frédéric Batteux, Manon Roynard, Yichao Shen, Mathieu Bourgey, Flore Rozenberg, Federica Sallusto, Peng Zhang, David Jarrossay, Carmen Oleaga-Quintas, Jean-Laurent Casanova, Daniela Latorre, Gaspard Kerner, Mahbuba Rahman, Houda Elarabi, Federico Mele, Yoann Seeleuthner, James P. Di Santo, Stuart G. Tangye, Michael S. Kobor, Janet Markle, Dusan Bogunovic, Stéphanie Boisson-Dupuis, Julia L. Maclsaac, Lucas T. Husquin, Lisa Worley, Conor Gruber, Cindy S. Ma, Jérémie Rosain, Taushif Khan, Thomas L. Carroll, Mohamed Jeljeli, Abderrahmane Errami, Anne Puel, Qiang Pan-Hammarström, Philippe Gros, Ibithal Benhsaien, Aziz Bousfiha, Fatima Ailal, Carys A. Croft, Rui Yang, Masato Ogishi, Rockefeller University [New York], Università della Svizzera italiana = University of Italian Switzerland (USI), Garvan Institute of medical research, McGill University = Université McGill [Montréal, Canada], Laboratory of Human Genetics of Infectious Diseases (Necker Branch - INSERM U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Université Hassan II [Casablanca] (UH2MC), Immunité Innée - Innate Immunity, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Cité (UPCité), Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich), Icahn School of Medicine at Mount Sinai [New York] (MSSM), We thank the patients and families, members of the laboratory, Cecilia Lindestam Arlehamn and Alessandro Sette, NIH Tetramer Core Facility (NTCF), James McCluskey, Jamie Rossjohn, and David Fairlie, the Genomics and the Flow Cytometry Resource Center of Rockefeller University, National Center for Advancing Translational Sciences of the National Institutes of Health (UL1TR001866 to Rockefeller University), Steven Elledge, National Institute of Allergy and Infectious Diseases (R37AI095983 to J.L.C. and U19AI118626 to F.S.), Sackler Center for Biomedicine and Nutrition at the Center for Clinical and Translational Science (CCTS), Shapiro-Silverberg Fund for the Advancement of Translational Research at CCTS, Rockefeller University (to R.Y.), Research Grant Program of the Immune Deficiency Foundation (to R.Y.), Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence (ANR-10-LABX-62-IBEID), French National Research Agency under the 'Investments for the future' program (ANR-10-IAHU-01), ANR-GENMSMD (ANR-16-CE17-0005-01 to J.B.), ANR-LTh-MSMD-CMCD (ANR-18-CE93-0008-01 to A.P and F.S.), Fonds de Recherche en Santé Respiratoire (SRC2017 to J.B.), French Foundation for Medical Research (FRM) (EQU201903007798), the SCOR Corporate Foundation for Science, ECOS Nord (C19S01-63407 to J.B.), Swiss National Science Foundation (310030L_182728 to F.S.), French Foundation for Medical Research (FRM) (EQU201903007798), Helmut Horten Foundation, Canadian Center for Computational Genomics (C3G), Genomics Technology Platform (GTP), and Genome Canada. J. R. was supported by INSERM Poste d’accueil and and Imagine Institute, T.K. by Qatar National Research Fund (PPM1-1220-150017). S.G.T. by Program grant (1113904), Principal Research Fellowship (1042925), and Leadership 3 Investigator grant (1176665) from the National Health and Medical Research Council of Australia, C.S.M. by an Early/Mid-Career Development Research Fellowship, Ministry of Health, NSW Government, R.Y. by Stony Wold-Herbert Fund., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), ANR-10-IAHU-0001,Imagine,Institut Hospitalo-Universitaire Imagine(2010), ANR-16-CE17-0005,GENMSMD,Dissection génétique de la Susceptibilité Mendélienne aux infections mycobactériennes chez l'homme(2016), ANR-18-CE93-0008,LTh-MSMD-CMCD,Différenciation des lymphocytes T-helper (Th) dans les défauts génétiques de l'immunité contre Mycobacterium et/ou Candida species.(2018), Garvan Institute of Medical Research [Darlinghurst, Australia], Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université de Paris (UP)

Subjects
Male, inborn errors of immunity, [SDV]Life Sciences [q-bio], Mendelian susceptibility to mycobacterial disease, MESH: Amino Acid Sequence, Adaptive Immunity, MESH: Base Sequence, Epigenesis, Genetic, mycobacterium, MESH: INDEL Mutation, 0302 clinical medicine, MESH: DNA Methylation, INDEL Mutation, Loss of Function Mutation, Interferon gamma, MESH: Epigenesis, Genetic, MESH: CpG Islands, IFN-γ, Immunodeficiency, 0303 health sciences, biology, MESH: Dendritic Cells, Homozygote, T-Lymphocytes, Helper-Inducer, MESH: Infant, Chromatin, Pedigree, 3. Good health, Killer Cells, Natural, Child, Preschool, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, MESH: Immunity, Innate, medicine.drug, MESH: Homozygote, MESH: Killer Cells, Natural, MESH: Pedigree, MESH: T-Box Domain Proteins, MESH: Interferon-gamma, T-bet, Article, General Biochemistry, Genetics and Molecular Biology, MESH: Chromatin, Interferon-gamma, 03 medical and health sciences, Immunity, medicine, MESH: Mycobacterium, Humans, Cell Lineage, Amino Acid Sequence, MESH: Mycobacterium Infections, MESH: T-Lymphocytes, Helper-Inducer, Transcription factor, 030304 developmental biology, Mycobacterium Infections, MESH: Humans, Base Sequence, MESH: Transcriptome, MESH: Child, Preschool, Infant, MESH: Loss of Function Mutation, Dendritic Cells, DNA Methylation, Mycobacterial disease, MESH: Cell Lineage, medicine.disease, biology.organism_classification, Immunity, Innate, MESH: Male, innate-like adaptive lymphocyte, Mycobacterial antigen, Immunology, CpG Islands, innate lymphocyte, T-Box Domain Proteins, Transcriptome, immunodeficiency, MESH: Female, 030217 neurology & neurosurgery, CD8, MESH: Adaptive Immunity, Mycobacterium
Abstract

International audience; Inborn errors of human interferon gamma (IFN-γ) immunity underlie mycobacterial disease. We report a patient with mycobacterial disease due to inherited deficiency of the transcription factor T-bet. The patient has extremely low counts of circulating Mycobacterium-reactive natural killer (NK), invariant NKT (iNKT), mucosal-associated invariant T (MAIT), and Vδ2+ γδ T lymphocytes, and of Mycobacterium-non reactive classic TH1 lymphocytes, with the residual populations of these cells also producing abnormally small amounts of IFN-γ. Other lymphocyte subsets develop normally but produce low levels of IFN-γ, with the exception of CD8+ αβ T and non-classic CD4+ αβ TH1∗ lymphocytes, which produce IFN-γ normally in response to mycobacterial antigens. Human T-bet deficiency thus underlies mycobacterial disease by preventing the development of innate (NK) and innate-like adaptive lymphocytes (iNKT, MAIT, and Vδ2+ γδ T cells) and IFN-γ production by them, with mycobacterium-specific, IFN-γ-producing, purely adaptive CD8+ αβ T, and CD4+ αβ TH1∗ cells unable to compensate for this deficit.

Published
2020
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7. Tissue-Resident Lymphocytes Across Innate and Adaptive Lineages

Author

Chun Chou and Ming O. Li

Subjects
0301 basic medicine, lcsh:Immunologic diseases. Allergy, Cell type, Lymphocyte, Immunology, conventional T cells, Context (language use), Review, Adaptive Immunity, Biology, Infections, Secondary lymphoid organs, 03 medical and health sciences, 0302 clinical medicine, Immune system, Neoplasms, medicine, Animals, Humans, Immunology and Allergy, cancer, Lymphocytes, tissue resident, innate-like T cells, Cancer, medicine.disease, Immunity, Innate, infection, 3. Good health, 030104 developmental biology, medicine.anatomical_structure, innate lymphocyte, lcsh:RC581-607, Homeostasis, 030215 immunology
Abstract

Lymphocytes are an integral component of the immune system. Classically, all lymphocytes were thought to perpetually recirculate between secondary lymphoid organs and only traffic to non-lymphoid tissues upon activation. In recent years, a diverse family of non-circulating lymphocytes have been identified. These include innate lymphocytes, innate-like T cells and a subset of conventional T cells. Spanning the innate-adaptive spectrum, these tissue-resident lymphocytes carry out specialized functions and cross-talk with other immune cell types to maintain tissue integrity and homeostasis both at the steady state and during pathological conditions. In this review, we provide an overview of the heterogeneous tissue-resident lymphocyte populations, discuss their development, and highlight their functions both in the context of microbial infection and cancer.

Published
2018
Full Text
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8. Group 2 Innate Lymphoid Cells (ILC2): Type 2 Immunity and Helminth Immunity

Author

De’Broski R. Herbert, Bonnie Douglas, and Kelly Zullo

Subjects
0301 basic medicine, Population, Helminthiasis, Inflammation, Review, Biology, Catalysis, lcsh:Chemistry, Inorganic Chemistry, Mice, 03 medical and health sciences, 0302 clinical medicine, Immunity, Helminths, medicine, Animals, Humans, Macrophage, Cell Lineage, Lymphocytes, Physical and Theoretical Chemistry, education, helminth, mucosa, lcsh:QH301-705.5, Molecular Biology, Spectroscopy, education.field_of_study, Goblet cell, Interleukin-13, Organic Chemistry, Innate lymphoid cell, type 2 immunity, General Medicine, Eosinophil, Mast cell, Immunity, Innate, 3. Good health, Computer Science Applications, 030104 developmental biology, medicine.anatomical_structure, lcsh:Biology (General), lcsh:QD1-999, Immunology, innate lymphocyte, Interleukin-5, medicine.symptom, 030215 immunology
Abstract

Group 2 innate lymphoid cells (ILC2) have emerged as a major component of type 2 inflammation in mice and humans. ILC2 secrete large amounts of interleukins 5 and 13, which are largely responsible for host protective immunity against helminth parasites because these cytokines induce profound changes in host physiology that include: goblet cell metaplasia, mucus accumulation, smooth muscle hypercontractility, eosinophil and mast cell recruitment, and alternative macrophage activation (M2). This review covers the initial recognition of ILC2 as a distinct cell lineage, the key studies that established their biological importance, particularly in helminth infection, and the new directions that are likely to be the focus of emerging work that further explores this unique cell population in the context of health and disease.

Published
2019
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9. A doppelgänger of T cell development

Author

Christelle Harly, Avinash Bhandoola, CHRISTELLE, HARLY, National Institutes of Health [Bethesda] (NIH), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), and 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)

Subjects
0301 basic medicine, T-Lymphocytes, T cell, Cellular differentiation, [SDV]Life Sciences [q-bio], Cell lineage, Editorials: Cell Cycle Features, Biology, 03 medical and health sciences, T-cell, T-Lymphocyte Subsets, Immunity, medicine, Humans, Cytotoxic T cell, Cell Lineage, Effector functions, skin and connective tissue diseases, Molecular Biology, development, ComputingMilieux_MISCELLANEOUS, Innate lymphoid cell, Cell Differentiation, Cell Biology, Immunity, Innate, Cell biology, body regions, [SDV] Life Sciences [q-bio], 030104 developmental biology, medicine.anatomical_structure, innate lymphocyte, Developmental Biology, Lymphocyte subsets
Abstract

Innate lymphoid cells (ILCs) were recently identified as the innate counterpart of adaptive T-cells, after the discovery of several ILC subsets with effector functions strikingly similar to T-cell ...

Published
2016
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