The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation
Innate lymphoid cells (ILCs) are tissue resident cells with organ-specific properties. Here, we show that the central nervous system (CNS) encompasses ILCs. In particular, CD3−NK1.1+ cells present in the murine CNS comprise natural killer (NK) cells, ILC1s, intermediate ILC1s (intILC1s) and ex-ILC3s...
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Frontiers Media S.A.
2019-10-01
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Series: | Frontiers in Immunology |
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Online Access: | https://www.frontiersin.org/article/10.3389/fimmu.2019.02337/full |
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author | Silvina Romero-Suárez Alba Del Rio Serrato Roemel Jeusep Bueno Daniel Brunotte-Strecker Christina Stehle Caio Andreeta Figueiredo Laura Hertwig Laura Hertwig Ildiko R. Dunay Chiara Romagnani Carmen Infante-Duarte |
author_facet | Silvina Romero-Suárez Alba Del Rio Serrato Roemel Jeusep Bueno Daniel Brunotte-Strecker Christina Stehle Caio Andreeta Figueiredo Laura Hertwig Laura Hertwig Ildiko R. Dunay Chiara Romagnani Carmen Infante-Duarte |
author_sort | Silvina Romero-Suárez |
collection | DOAJ |
description | Innate lymphoid cells (ILCs) are tissue resident cells with organ-specific properties. Here, we show that the central nervous system (CNS) encompasses ILCs. In particular, CD3−NK1.1+ cells present in the murine CNS comprise natural killer (NK) cells, ILC1s, intermediate ILC1s (intILC1s) and ex-ILC3s. We investigated the properties of CNS-ILC1s in comparison with CNS-NK cells during steady state and experimental autoimmune encephalomyelitis (EAE). ILC1s characteristically express CXCR3, CXCR6, DNAM-1, TRAIL, and CD200R and display heightened TNF-α production upon stimulation. In addition, ILC1s express perforin and are able to degranulate, although in a lesser extent than NK cells. Within the CNS compartments, ILC1s are enriched in the choroid plexus where very few NK cells are present, and also reside in the brain parenchyma and meninges. During EAE, ILC1s maintain stable IFN-γ and TNF-α levels while in NK cells the production of these cytokines increases as EAE progresses. Moreover, the amount of ILC1s and intILC1s increase in the parenchyma during EAE, but in contrast to NK cells, they show no signs of local proliferation. The upregulation in the inflamed brain of chemokines involved in ILC1 migration, such as CXCL9, CXCL10, and CXCL16 may lead to a recruitment of ILC1s from meninges or choroid plexus into the brain parenchyma. In sum, CNS-ILC1 phenotype, distribution and moderate inflammatory response during EAE suggest that they may act as gatekeepers involved in the control of neuroinflammation. |
first_indexed | 2024-12-13T13:06:45Z |
format | Article |
id | doaj.art-cffee1e659144451aed1172d0e8b298d |
institution | Directory Open Access Journal |
issn | 1664-3224 |
language | English |
last_indexed | 2024-12-13T13:06:45Z |
publishDate | 2019-10-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Immunology |
spelling | doaj.art-cffee1e659144451aed1172d0e8b298d2022-12-21T23:44:48ZengFrontiers Media S.A.Frontiers in Immunology1664-32242019-10-011010.3389/fimmu.2019.02337472226The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to InflammationSilvina Romero-Suárez0Alba Del Rio Serrato1Roemel Jeusep Bueno2Daniel Brunotte-Strecker3Christina Stehle4Caio Andreeta Figueiredo5Laura Hertwig6Laura Hertwig7Ildiko R. Dunay8Chiara Romagnani9Carmen Infante-Duarte10Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute for Medical Immunology, Berlin, GermanyCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute for Medical Immunology, Berlin, GermanyCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute for Medical Immunology, Berlin, GermanyCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute for Medical Immunology, Berlin, GermanyInnate Immunity, German Rheumatism Research Center (DRFZ), Leibniz Association, Berlin, GermanyMedical Faculty, Institute of Inflammation and Neurodegeneration, Otto von Guericke University Magdeburg, Magdeburg, GermanyCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute for Medical Immunology, Berlin, GermanyDepartment of Medicine Huddinge, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, SwedenMedical Faculty, Institute of Inflammation and Neurodegeneration, Otto von Guericke University Magdeburg, Magdeburg, GermanyInnate Immunity, German Rheumatism Research Center (DRFZ), Leibniz Association, Berlin, GermanyCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Institute for Medical Immunology, Berlin, GermanyInnate lymphoid cells (ILCs) are tissue resident cells with organ-specific properties. Here, we show that the central nervous system (CNS) encompasses ILCs. In particular, CD3−NK1.1+ cells present in the murine CNS comprise natural killer (NK) cells, ILC1s, intermediate ILC1s (intILC1s) and ex-ILC3s. We investigated the properties of CNS-ILC1s in comparison with CNS-NK cells during steady state and experimental autoimmune encephalomyelitis (EAE). ILC1s characteristically express CXCR3, CXCR6, DNAM-1, TRAIL, and CD200R and display heightened TNF-α production upon stimulation. In addition, ILC1s express perforin and are able to degranulate, although in a lesser extent than NK cells. Within the CNS compartments, ILC1s are enriched in the choroid plexus where very few NK cells are present, and also reside in the brain parenchyma and meninges. During EAE, ILC1s maintain stable IFN-γ and TNF-α levels while in NK cells the production of these cytokines increases as EAE progresses. Moreover, the amount of ILC1s and intILC1s increase in the parenchyma during EAE, but in contrast to NK cells, they show no signs of local proliferation. The upregulation in the inflamed brain of chemokines involved in ILC1 migration, such as CXCL9, CXCL10, and CXCL16 may lead to a recruitment of ILC1s from meninges or choroid plexus into the brain parenchyma. In sum, CNS-ILC1 phenotype, distribution and moderate inflammatory response during EAE suggest that they may act as gatekeepers involved in the control of neuroinflammation.https://www.frontiersin.org/article/10.3389/fimmu.2019.02337/fullinnate lymphoid cells (ILCs)ILC1snatural killer (NK) cellscentral nervous system (CNS)experimental autoimmune encephalomyelitis (EAE)mouse |
spellingShingle | Silvina Romero-Suárez Alba Del Rio Serrato Roemel Jeusep Bueno Daniel Brunotte-Strecker Christina Stehle Caio Andreeta Figueiredo Laura Hertwig Laura Hertwig Ildiko R. Dunay Chiara Romagnani Carmen Infante-Duarte The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation Frontiers in Immunology innate lymphoid cells (ILCs) ILC1s natural killer (NK) cells central nervous system (CNS) experimental autoimmune encephalomyelitis (EAE) mouse |
title | The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation |
title_full | The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation |
title_fullStr | The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation |
title_full_unstemmed | The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation |
title_short | The Central Nervous System Contains ILC1s That Differ From NK Cells in the Response to Inflammation |
title_sort | central nervous system contains ilc1s that differ from nk cells in the response to inflammation |
topic | innate lymphoid cells (ILCs) ILC1s natural killer (NK) cells central nervous system (CNS) experimental autoimmune encephalomyelitis (EAE) mouse |
url | https://www.frontiersin.org/article/10.3389/fimmu.2019.02337/full |
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