TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production
The DNA binding protein AT-rich interacting domain 3a (ARID3a)22ARID3a, AT-rich interacting domain 3a is expressed in healthy human hematopoietic cord blood progenitors where its modulation influences myeloid versus B lineage development. ARID3a is also variably expressed in subsets of adult periphe...
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Veröffentlicht in: | Cellular immunology 2020-11, Vol.357, p.104201-104201, Article 104201 |
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description | The DNA binding protein AT-rich interacting domain 3a (ARID3a)22ARID3a, AT-rich interacting domain 3a is expressed in healthy human hematopoietic cord blood progenitors where its modulation influences myeloid versus B lineage development. ARID3a is also variably expressed in subsets of adult peripheral blood hematopoietic progenitors where the consequences of ARID3a expression are unknown. In B lymphocytes, Toll-like receptor (TLR)33TLR, Toll-like receptor signaling induces ARID3a expression in association with Type I interferon inflammatory cytokines. We hypothesized that TLR ligand stimulation of peripheral blood hematopoietic progenitors would induce ARID3a expression resulting in interferon production, and potentially influencing lineage decisions. Our data revealed that the TLR9 agonist CpG induces ARID3a expression with interferon alpha synthesis in human hematopoietic progenitors. However, ARID3a expression was not associated with increased B lineage development. These results demonstrate the need for further experiments to better define how pathogen-associated responses influence hematopoiesis. |
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ARID3a is also variably expressed in subsets of adult peripheral blood hematopoietic progenitors where the consequences of ARID3a expression are unknown. In B lymphocytes, Toll-like receptor (TLR)33TLR, Toll-like receptor signaling induces ARID3a expression in association with Type I interferon inflammatory cytokines. We hypothesized that TLR ligand stimulation of peripheral blood hematopoietic progenitors would induce ARID3a expression resulting in interferon production, and potentially influencing lineage decisions. Our data revealed that the TLR9 agonist CpG induces ARID3a expression with interferon alpha synthesis in human hematopoietic progenitors. However, ARID3a expression was not associated with increased B lineage development. These results demonstrate the need for further experiments to better define how pathogen-associated responses influence hematopoiesis.</description><identifier>ISSN: 0008-8749</identifier><identifier>EISSN: 1090-2163</identifier><identifier>DOI: 10.1016/j.cellimm.2020.104201</identifier><identifier>PMID: 32979763</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Adult ; ARID3a ; B-Lymphocytes - cytology ; B-Lymphocytes - metabolism ; CpG Islands ; Cytokines - metabolism ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - biosynthesis ; DNA-Binding Proteins - blood ; Female ; Flow Cytometry - methods ; Gene Expression ; Hematopoiesis ; Hematopoietic Stem Cells - cytology ; Hematopoietic Stem Cells - drug effects ; Hematopoietic Stem Cells - metabolism ; Humans ; Innate immunity ; Interferon-alpha - biosynthesis ; Interferon-alpha - genetics ; Interferon-alpha - immunology ; Ligands ; Middle Aged ; Signal Transduction ; Toll-Like Receptors - blood ; Transcription Factors - antagonists & inhibitors ; Transcription Factors - biosynthesis ; Transcription Factors - blood</subject><ispartof>Cellular immunology, 2020-11, Vol.357, p.104201-104201, Article 104201</ispartof><rights>2020 The Author(s)</rights><rights>Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-7d6ff77ee190e99353d8e98ac7b44cf8e7ef576a845d69e9dd465c56ddce84e83</citedby><cites>FETCH-LOGICAL-c467t-7d6ff77ee190e99353d8e98ac7b44cf8e7ef576a845d69e9dd465c56ddce84e83</cites><orcidid>0000-0002-3923-7342 ; 0000-0002-9308-237X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cellimm.2020.104201$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32979763$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ratliff, Michelle L.</creatorcontrib><creatorcontrib>Shankar, Malini</creatorcontrib><creatorcontrib>Guthridge, Joel M.</creatorcontrib><creatorcontrib>James, Judith A.</creatorcontrib><creatorcontrib>Webb, Carol F.</creatorcontrib><title>TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production</title><title>Cellular immunology</title><addtitle>Cell Immunol</addtitle><description>The DNA binding protein AT-rich interacting domain 3a (ARID3a)22ARID3a, AT-rich interacting domain 3a is expressed in healthy human hematopoietic cord blood progenitors where its modulation influences myeloid versus B lineage development. ARID3a is also variably expressed in subsets of adult peripheral blood hematopoietic progenitors where the consequences of ARID3a expression are unknown. In B lymphocytes, Toll-like receptor (TLR)33TLR, Toll-like receptor signaling induces ARID3a expression in association with Type I interferon inflammatory cytokines. We hypothesized that TLR ligand stimulation of peripheral blood hematopoietic progenitors would induce ARID3a expression resulting in interferon production, and potentially influencing lineage decisions. Our data revealed that the TLR9 agonist CpG induces ARID3a expression with interferon alpha synthesis in human hematopoietic progenitors. However, ARID3a expression was not associated with increased B lineage development. These results demonstrate the need for further experiments to better define how pathogen-associated responses influence hematopoiesis.</description><subject>Adult</subject><subject>ARID3a</subject><subject>B-Lymphocytes - cytology</subject><subject>B-Lymphocytes - metabolism</subject><subject>CpG Islands</subject><subject>Cytokines - metabolism</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - biosynthesis</subject><subject>DNA-Binding Proteins - blood</subject><subject>Female</subject><subject>Flow Cytometry - methods</subject><subject>Gene Expression</subject><subject>Hematopoiesis</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>Hematopoietic Stem Cells - drug effects</subject><subject>Hematopoietic Stem Cells - metabolism</subject><subject>Humans</subject><subject>Innate immunity</subject><subject>Interferon-alpha - biosynthesis</subject><subject>Interferon-alpha - genetics</subject><subject>Interferon-alpha - immunology</subject><subject>Ligands</subject><subject>Middle Aged</subject><subject>Signal Transduction</subject><subject>Toll-Like Receptors - blood</subject><subject>Transcription Factors - antagonists & inhibitors</subject><subject>Transcription Factors - biosynthesis</subject><subject>Transcription Factors - blood</subject><issn>0008-8749</issn><issn>1090-2163</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9uEzEQxi1ERUPhEUB75LLB3vX6zwVUFQqRoiJV5Ww59mziaNcOtrdSH4sX4ZnwKqGip54sz3zfN6P5IfSO4CXBhH3cLw0MgxvHZYObuUYbTF6gBcES1w1h7Uu0wBiLWnAqz9HrlPYYE0IlfoXO20ZyyVm7QHC3vq3Ab_UWRvC5ct5OBlJ1ebv60uryrXbTqH21GUKw1Q5GncMhOMjOVIcYtuBdDjFV2ttqDHYadC7u1fXNn99zv4RlF_wbdNbrIcHb03uBfl5_vbv6Xq9_fFtdXa5rQxnPNbes7zkHIBKDlG3XWgFSaMM3lJpeAIe-40wL2lkmQVpLWWc6Zq0BQUG0F-jTMfcwbUYoVZ-jHtQhulHHBxW0U0873u3UNtwrzlveUFoCPpwCYvg1QcpqdGk-tPYQpqSKhjHOpGBF2h2lJoaUIvSPYwhWMyK1VydEakakjoiK7_3_Oz66_jEpgs9HAZRL3TuIKhkH3oB1EUxWNrhnRvwFLaGoVg</recordid><startdate>20201101</startdate><enddate>20201101</enddate><creator>Ratliff, Michelle L.</creator><creator>Shankar, Malini</creator><creator>Guthridge, Joel M.</creator><creator>James, Judith A.</creator><creator>Webb, Carol F.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3923-7342</orcidid><orcidid>https://orcid.org/0000-0002-9308-237X</orcidid></search><sort><creationdate>20201101</creationdate><title>TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production</title><author>Ratliff, Michelle L. ; Shankar, Malini ; Guthridge, Joel M. ; James, Judith A. ; Webb, Carol F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-7d6ff77ee190e99353d8e98ac7b44cf8e7ef576a845d69e9dd465c56ddce84e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>ARID3a</topic><topic>B-Lymphocytes - cytology</topic><topic>B-Lymphocytes - metabolism</topic><topic>CpG Islands</topic><topic>Cytokines - metabolism</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - biosynthesis</topic><topic>DNA-Binding Proteins - blood</topic><topic>Female</topic><topic>Flow Cytometry - methods</topic><topic>Gene Expression</topic><topic>Hematopoiesis</topic><topic>Hematopoietic Stem Cells - cytology</topic><topic>Hematopoietic Stem Cells - drug effects</topic><topic>Hematopoietic Stem Cells - metabolism</topic><topic>Humans</topic><topic>Innate immunity</topic><topic>Interferon-alpha - biosynthesis</topic><topic>Interferon-alpha - genetics</topic><topic>Interferon-alpha - immunology</topic><topic>Ligands</topic><topic>Middle Aged</topic><topic>Signal Transduction</topic><topic>Toll-Like Receptors - blood</topic><topic>Transcription Factors - antagonists & inhibitors</topic><topic>Transcription Factors - biosynthesis</topic><topic>Transcription Factors - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ratliff, Michelle L.</creatorcontrib><creatorcontrib>Shankar, Malini</creatorcontrib><creatorcontrib>Guthridge, Joel M.</creatorcontrib><creatorcontrib>James, Judith A.</creatorcontrib><creatorcontrib>Webb, Carol F.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ratliff, Michelle L.</au><au>Shankar, Malini</au><au>Guthridge, Joel M.</au><au>James, Judith A.</au><au>Webb, Carol F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production</atitle><jtitle>Cellular immunology</jtitle><addtitle>Cell Immunol</addtitle><date>2020-11-01</date><risdate>2020</risdate><volume>357</volume><spage>104201</spage><epage>104201</epage><pages>104201-104201</pages><artnum>104201</artnum><issn>0008-8749</issn><eissn>1090-2163</eissn><abstract>The DNA binding protein AT-rich interacting domain 3a (ARID3a)22ARID3a, AT-rich interacting domain 3a is expressed in healthy human hematopoietic cord blood progenitors where its modulation influences myeloid versus B lineage development. ARID3a is also variably expressed in subsets of adult peripheral blood hematopoietic progenitors where the consequences of ARID3a expression are unknown. In B lymphocytes, Toll-like receptor (TLR)33TLR, Toll-like receptor signaling induces ARID3a expression in association with Type I interferon inflammatory cytokines. We hypothesized that TLR ligand stimulation of peripheral blood hematopoietic progenitors would induce ARID3a expression resulting in interferon production, and potentially influencing lineage decisions. Our data revealed that the TLR9 agonist CpG induces ARID3a expression with interferon alpha synthesis in human hematopoietic progenitors. However, ARID3a expression was not associated with increased B lineage development. 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subjects | Adult ARID3a B-Lymphocytes - cytology B-Lymphocytes - metabolism CpG Islands Cytokines - metabolism DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - biosynthesis DNA-Binding Proteins - blood Female Flow Cytometry - methods Gene Expression Hematopoiesis Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - drug effects Hematopoietic Stem Cells - metabolism Humans Innate immunity Interferon-alpha - biosynthesis Interferon-alpha - genetics Interferon-alpha - immunology Ligands Middle Aged Signal Transduction Toll-Like Receptors - blood Transcription Factors - antagonists & inhibitors Transcription Factors - biosynthesis Transcription Factors - blood |
title | TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production |
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