Myeloid - derived suppressor cells in Type 1 diabetes are an expanded population exhibiting diverse T-cell suppressor mechanisms
Myeloid-derived suppressor cells (MDSC) represent a heterogeneous group of immature myeloid cells with immunoregulatory function in cancer and autoimmune diseases. In humans, two subsets of MDSC were determined based on the characteristic surface markers, monocytic MDSC (M-MDSC) and granulocytic MDS...
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| creator | Grohová, Anna Dáňová, Klára Adkins, Irena Šumník, Zdeněk Petruželková, Lenka Obermannová, Barbora Koloušková, Stanislava Špíšek, Radek Palová-Jelínková, Lenka |
| description | Myeloid-derived suppressor cells (MDSC) represent a heterogeneous group of immature myeloid cells with immunoregulatory function in cancer and autoimmune diseases. In humans, two subsets of MDSC were determined based on the characteristic surface markers, monocytic MDSC (M-MDSC) and granulocytic MDSC (G-MDSC). Expansion of MDSC has been reported in some murine models and patients with autoimmune diseases and their immune-suppressive properties were characterized. However, the exact role of MDSC in the pathogenesis of autoimmune diseases is more complex and/or controversial. In type 1 diabetes mellitus (T1D), the increased frequency of MDSC was found in the blood of T1D patients but their suppressor capacity was diminished. In our study, we assessed the role of M-MDSC in the pathogenesis of T1D and showed for the first time the increased frequency of M-MDSC not only in the blood of T1D patients but also in their at-risk relatives compared to healthy donors. T1D patients with inadequate long term metabolic control showed an elevation of M-MDSC compared to patients with better disease control. Furthermore, we described the positive correlation between the percentage of M-MDSC and Th17 cells and IFN-γ producing T cells in T1D patients and their at-risk relatives. Finally, we found that the ability of M-MDSC to suppress autologous T cells is efficient only at the high MDSC: T cells ratio and dependent on cell-cell-contact and TGF-β production. Our data show that the engagement of MDSC in the pathogenesis of T1D is evident, yet not entirely explored and more experiments are required to clarify whether MDSC are beneficial or harmful in T1D. |
| doi_str_mv | 10.1371/journal.pone.0242092 |
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In humans, two subsets of MDSC were determined based on the characteristic surface markers, monocytic MDSC (M-MDSC) and granulocytic MDSC (G-MDSC). Expansion of MDSC has been reported in some murine models and patients with autoimmune diseases and their immune-suppressive properties were characterized. However, the exact role of MDSC in the pathogenesis of autoimmune diseases is more complex and/or controversial. In type 1 diabetes mellitus (T1D), the increased frequency of MDSC was found in the blood of T1D patients but their suppressor capacity was diminished. In our study, we assessed the role of M-MDSC in the pathogenesis of T1D and showed for the first time the increased frequency of M-MDSC not only in the blood of T1D patients but also in their at-risk relatives compared to healthy donors. T1D patients with inadequate long term metabolic control showed an elevation of M-MDSC compared to patients with better disease control. Furthermore, we described the positive correlation between the percentage of M-MDSC and Th17 cells and IFN-γ producing T cells in T1D patients and their at-risk relatives. Finally, we found that the ability of M-MDSC to suppress autologous T cells is efficient only at the high MDSC: T cells ratio and dependent on cell-cell-contact and TGF-β production. Our data show that the engagement of MDSC in the pathogenesis of T1D is evident, yet not entirely explored and more experiments are required to clarify whether MDSC are beneficial or harmful in T1D.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0242092</identifier><identifier>PMID: 33206686</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adolescent ; Age ; Analysis ; Animal models ; Autoimmune diseases ; Biological markers ; Biology and Life Sciences ; Blood ; Cancer ; CD4 Lymphocyte Count ; Child ; Development and progression ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Type 1 - blood ; Diabetes Mellitus, Type 1 - immunology ; Diagnosis ; Disease ; Disease control ; Female ; Glucose ; Helper cells ; Hemoglobin ; Hospitals ; Humans ; Immunology ; Immunoregulation ; Interferon-gamma - metabolism ; Lymphocytes ; Lymphocytes T ; Male ; Medicine ; Medicine and Health Sciences ; Metabolism ; Monocytes ; Myeloid cells ; Myeloid-Derived Suppressor Cells - immunology ; Pathogenesis ; Pediatrics ; Physiological aspects ; Risk factors ; Suppressor cells ; Surface markers ; T cells ; T-Lymphocytes, Regulatory - immunology ; Th17 Cells - immunology ; Type 1 diabetes ; γ-Interferon</subject><ispartof>PloS one, 2020-11, Vol.15 (11), p.e0242092-e0242092</ispartof><rights>COPYRIGHT 2020 Public Library of Science</rights><rights>2020 Grohová et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Furthermore, we described the positive correlation between the percentage of M-MDSC and Th17 cells and IFN-γ producing T cells in T1D patients and their at-risk relatives. Finally, we found that the ability of M-MDSC to suppress autologous T cells is efficient only at the high MDSC: T cells ratio and dependent on cell-cell-contact and TGF-β production. 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metabolism</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metabolism</subject><subject>Monocytes</subject><subject>Myeloid cells</subject><subject>Myeloid-Derived Suppressor Cells - immunology</subject><subject>Pathogenesis</subject><subject>Pediatrics</subject><subject>Physiological aspects</subject><subject>Risk factors</subject><subject>Suppressor cells</subject><subject>Surface markers</subject><subject>T cells</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Th17 Cells - immunology</subject><subject>Type 1 diabetes</subject><subject>γ-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QDguhFxzRJ0-ZGWBY_BlYWdPQ2pM3JTJZOU5N22Lnzp5vudJep7IXkIuHked-TnOQkycsMLzJaZB-u3eBb1Sw618ICE0awII-S00xQknKC6eOj9UnyLIRrjHNacv40OaGUYM5Lfpr8-baHxlmNUqTB2x1oFIau8xCC86iGpgnItmi17wBlSFtVQQ8BKQ9ItQhuOtXqqOlcNzSqt26MbWxle9uuI74DHwCt0tHo2HgL9Ua1NmzD8-SJUU2AF9N8lvz8_Gl18TW9vPqyvDi_TGsuSJ_q0mSG4tpwynSpOS2ZynSd1wQXQhDABdYGKmy4AaJ4YYghJYVcFAqywhh6lrw--HaNC3IqXpCE8UyIIi9ZJJYHQjt1LTtvt8rvpVNW3gacX0vle1s3IFmOTaV5XpdCsLwSQkHO8jxmYrhUhYheH6dsQ7UFXUPbe9XMTOc7rd3ItdvJgheUiSIavJsMvPs9QOjl1oaxiqoFN9yem7AM5wJH9M0_6MO3m6i1ihewrXExbz2aynPOSJZzzMdzLx6g4tCwtXX8acbG-EzwfiaITA83_VoNIcjlj-__z179mrNvj9gNqKbfBNcM4xcLc5AdwNq7EDyY-yJnWI6NclcNOTaKnBolyl4dP9C96K4z6F8jcA89</recordid><startdate>20201118</startdate><enddate>20201118</enddate><creator>Grohová, Anna</creator><creator>Dáňová, Klára</creator><creator>Adkins, Irena</creator><creator>Šumník, Zdeněk</creator><creator>Petruželková, Lenka</creator><creator>Obermannová, Barbora</creator><creator>Koloušková, Stanislava</creator><creator>Špíšek, Radek</creator><creator>Palová-Jelínková, Lenka</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1829-0758</orcidid></search><sort><creationdate>20201118</creationdate><title>Myeloid - 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blood</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diagnosis</topic><topic>Disease</topic><topic>Disease control</topic><topic>Female</topic><topic>Glucose</topic><topic>Helper cells</topic><topic>Hemoglobin</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunology</topic><topic>Immunoregulation</topic><topic>Interferon-gamma - metabolism</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Metabolism</topic><topic>Monocytes</topic><topic>Myeloid cells</topic><topic>Myeloid-Derived Suppressor Cells - immunology</topic><topic>Pathogenesis</topic><topic>Pediatrics</topic><topic>Physiological aspects</topic><topic>Risk factors</topic><topic>Suppressor cells</topic><topic>Surface markers</topic><topic>T cells</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Th17 Cells - immunology</topic><topic>Type 1 diabetes</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grohová, Anna</creatorcontrib><creatorcontrib>Dáňová, Klára</creatorcontrib><creatorcontrib>Adkins, Irena</creatorcontrib><creatorcontrib>Šumník, Zdeněk</creatorcontrib><creatorcontrib>Petruželková, Lenka</creatorcontrib><creatorcontrib>Obermannová, Barbora</creatorcontrib><creatorcontrib>Koloušková, Stanislava</creatorcontrib><creatorcontrib>Špíšek, Radek</creatorcontrib><creatorcontrib>Palová-Jelínková, Lenka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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In humans, two subsets of MDSC were determined based on the characteristic surface markers, monocytic MDSC (M-MDSC) and granulocytic MDSC (G-MDSC). Expansion of MDSC has been reported in some murine models and patients with autoimmune diseases and their immune-suppressive properties were characterized. However, the exact role of MDSC in the pathogenesis of autoimmune diseases is more complex and/or controversial. In type 1 diabetes mellitus (T1D), the increased frequency of MDSC was found in the blood of T1D patients but their suppressor capacity was diminished. In our study, we assessed the role of M-MDSC in the pathogenesis of T1D and showed for the first time the increased frequency of M-MDSC not only in the blood of T1D patients but also in their at-risk relatives compared to healthy donors. T1D patients with inadequate long term metabolic control showed an elevation of M-MDSC compared to patients with better disease control. Furthermore, we described the positive correlation between the percentage of M-MDSC and Th17 cells and IFN-γ producing T cells in T1D patients and their at-risk relatives. Finally, we found that the ability of M-MDSC to suppress autologous T cells is efficient only at the high MDSC: T cells ratio and dependent on cell-cell-contact and TGF-β production. Our data show that the engagement of MDSC in the pathogenesis of T1D is evident, yet not entirely explored and more experiments are required to clarify whether MDSC are beneficial or harmful in T1D.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>33206686</pmid><doi>10.1371/journal.pone.0242092</doi><tpages>e0242092</tpages><orcidid>https://orcid.org/0000-0003-1829-0758</orcidid><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_plos_journals_2461997584 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adolescent Age Analysis Animal models Autoimmune diseases Biological markers Biology and Life Sciences Blood Cancer CD4 Lymphocyte Count Child Development and progression Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Diabetes Mellitus, Type 1 - blood Diabetes Mellitus, Type 1 - immunology Diagnosis Disease Disease control Female Glucose Helper cells Hemoglobin Hospitals Humans Immunology Immunoregulation Interferon-gamma - metabolism Lymphocytes Lymphocytes T Male Medicine Medicine and Health Sciences Metabolism Monocytes Myeloid cells Myeloid-Derived Suppressor Cells - immunology Pathogenesis Pediatrics Physiological aspects Risk factors Suppressor cells Surface markers T cells T-Lymphocytes, Regulatory - immunology Th17 Cells - immunology Type 1 diabetes γ-Interferon |
| title | Myeloid - derived suppressor cells in Type 1 diabetes are an expanded population exhibiting diverse T-cell suppressor mechanisms |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T07%3A01%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Myeloid%20-%20derived%20suppressor%20cells%20in%20Type%201%20diabetes%20are%20an%20expanded%20population%20exhibiting%20diverse%20T-cell%20suppressor%20mechanisms&rft.jtitle=PloS%20one&rft.au=Grohov%C3%A1,%20Anna&rft.date=2020-11-18&rft.volume=15&rft.issue=11&rft.spage=e0242092&rft.epage=e0242092&rft.pages=e0242092-e0242092&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0242092&rft_dat=%3Cgale_plos_%3EA642156069%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2461997584&rft_id=info:pmid/33206686&rft_galeid=A642156069&rft_doaj_id=oai_doaj_org_article_450fbd65c89945b99ae5455e17408a79&rfr_iscdi=true |