IFN-stimulated gene LY6E in monocytes regulates the CD14/TLR4 pathway but inadequately restrains the hyperactivation of monocytes during chronic HIV-1 infection
Owing to ongoing recognition of pathogen-associated molecular patterns, immune activation and upregulation of IFN-stimulated genes (ISGs) are sustained in the chronically infected host. Albeit most ISGs are important effectors for containing viral replication, some might exert compensatory immune su...
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| Veröffentlicht in: | The Journal of immunology (1950) 2014-10, Vol.193 (8), p.4125-4136 |
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| container_title | The Journal of immunology (1950) |
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| creator | Xu, Xuan Qiu, Chao Zhu, Lingyan Huang, Jun Li, Lishuang Fu, Weihui Zhang, Linxia Wei, Jun Wang, Ying Geng, Yunqi Zhang, Xiaoyan Qiao, Wentao Xu, Jianqing |
| description | Owing to ongoing recognition of pathogen-associated molecular patterns, immune activation and upregulation of IFN-stimulated genes (ISGs) are sustained in the chronically infected host. Albeit most ISGs are important effectors for containing viral replication, some might exert compensatory immune suppression to limit pathological dysfunctions, although the mechanisms are not fully understood. In this study, we report that the ISG lymphocyte Ag 6 complex, locus E (LY6E) is a negative immune regulator of monocytes. LY6E in monocytes negatively modulated CD14 expression and subsequently dampened the responsiveness to LPS stimulation in vitro. In the setting of chronic HIV infection, the upregulation of LY6E was correlated with reduced CD14 level on monocytes; however, the immunosuppressive effect of LY6E was not adequate to remedy the hyperresponsiveness of activated monocytes. Taken together, the regulatory LY6E pathway in monocytes represents one of negative feedback mechanisms that counterbalance monocyte activation, which might be caused by LPS translocation through the compromised gastrointestinal tract during persistent HIV-1 infection and may serve as a potential target for immune intervention. |
| doi_str_mv | 10.4049/jimmunol.1401249 |
| format | Article |
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Albeit most ISGs are important effectors for containing viral replication, some might exert compensatory immune suppression to limit pathological dysfunctions, although the mechanisms are not fully understood. In this study, we report that the ISG lymphocyte Ag 6 complex, locus E (LY6E) is a negative immune regulator of monocytes. LY6E in monocytes negatively modulated CD14 expression and subsequently dampened the responsiveness to LPS stimulation in vitro. In the setting of chronic HIV infection, the upregulation of LY6E was correlated with reduced CD14 level on monocytes; however, the immunosuppressive effect of LY6E was not adequate to remedy the hyperresponsiveness of activated monocytes. Taken together, the regulatory LY6E pathway in monocytes represents one of negative feedback mechanisms that counterbalance monocyte activation, which might be caused by LPS translocation through the compromised gastrointestinal tract during persistent HIV-1 infection and may serve as a potential target for immune intervention.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1401249</identifier><identifier>PMID: 25225669</identifier><language>eng</language><publisher>United States</publisher><subject>Adult ; Antigens, Surface - genetics ; Antigens, Surface - immunology ; Cell Line, Tumor ; Female ; Gastrointestinal Tract - immunology ; GPI-Linked Proteins - genetics ; GPI-Linked Proteins - immunology ; HeLa Cells ; HIV Infections - immunology ; HIV Infections - virology ; HIV-1 - immunology ; Human immunodeficiency virus ; Human immunodeficiency virus 1 ; Humans ; Immune Tolerance ; Interferon Regulatory Factors - genetics ; Interferon-alpha - immunology ; Interferon-alpha - pharmacology ; Lentivirus ; Lipopolysaccharide Receptors - biosynthesis ; Lipopolysaccharide Receptors - immunology ; Lipopolysaccharides - immunology ; Male ; Middle Aged ; Monocytes - immunology ; RNA Interference ; RNA, Small Interfering ; Signal Transduction - immunology ; Toll-Like Receptor 4 - immunology ; Tumor Necrosis Factor-alpha - biosynthesis ; Up-Regulation ; Virus Replication - immunology</subject><ispartof>The Journal of immunology (1950), 2014-10, Vol.193 (8), p.4125-4136</ispartof><rights>Copyright © 2014 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-80bcafeb3e314981337125e4b8e78ab7abdd8bef326de449dfa8d24285a4e8523</citedby><cites>FETCH-LOGICAL-c440t-80bcafeb3e314981337125e4b8e78ab7abdd8bef326de449dfa8d24285a4e8523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25225669$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Xuan</creatorcontrib><creatorcontrib>Qiu, Chao</creatorcontrib><creatorcontrib>Zhu, Lingyan</creatorcontrib><creatorcontrib>Huang, Jun</creatorcontrib><creatorcontrib>Li, Lishuang</creatorcontrib><creatorcontrib>Fu, Weihui</creatorcontrib><creatorcontrib>Zhang, Linxia</creatorcontrib><creatorcontrib>Wei, Jun</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Geng, Yunqi</creatorcontrib><creatorcontrib>Zhang, Xiaoyan</creatorcontrib><creatorcontrib>Qiao, Wentao</creatorcontrib><creatorcontrib>Xu, Jianqing</creatorcontrib><title>IFN-stimulated gene LY6E in monocytes regulates the CD14/TLR4 pathway but inadequately restrains the hyperactivation of monocytes during chronic HIV-1 infection</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Owing to ongoing recognition of pathogen-associated molecular patterns, immune activation and upregulation of IFN-stimulated genes (ISGs) are sustained in the chronically infected host. 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Taken together, the regulatory LY6E pathway in monocytes represents one of negative feedback mechanisms that counterbalance monocyte activation, which might be caused by LPS translocation through the compromised gastrointestinal tract during persistent HIV-1 infection and may serve as a potential target for immune intervention.</description><subject>Adult</subject><subject>Antigens, Surface - genetics</subject><subject>Antigens, Surface - immunology</subject><subject>Cell Line, Tumor</subject><subject>Female</subject><subject>Gastrointestinal Tract - immunology</subject><subject>GPI-Linked Proteins - genetics</subject><subject>GPI-Linked Proteins - immunology</subject><subject>HeLa Cells</subject><subject>HIV Infections - immunology</subject><subject>HIV Infections - virology</subject><subject>HIV-1 - immunology</subject><subject>Human immunodeficiency virus</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Immune Tolerance</subject><subject>Interferon Regulatory Factors - genetics</subject><subject>Interferon-alpha - immunology</subject><subject>Interferon-alpha - pharmacology</subject><subject>Lentivirus</subject><subject>Lipopolysaccharide Receptors - biosynthesis</subject><subject>Lipopolysaccharide Receptors - immunology</subject><subject>Lipopolysaccharides - immunology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Monocytes - immunology</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Signal Transduction - immunology</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Up-Regulation</subject><subject>Virus Replication - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFr2zAYhsVYWdN2952Gjru4lWRJlo8ja9dA2KB0g56MLH1OVGwpleQO_5v91DlNOnbb6bs8z8MHL0IfKLnkhNdXj24YRh_6S8oJZbx-gxZUCFJISeRbtCCEsYJWsjpFZyk9EkIkYfwdOmWCMSFlvUC_VzffipTdMPY6g8Ub8IDXD_IaO4-H4IOZMiQcYfMCJJy3gJdfKL-6X99xvNN5-0tPuB3zLGgLT-NM9dMspBy18wdhO-0gapPds84ueBy6f9p2jM5vsNnG4J3Bt6ufBZ1jHZg9e4FOOt0neH-85-jHzfX98rZYf_-6Wn5eF4ZzkgtFWqM7aEsoKa8VLcuKMgG8VVAp3Va6tVa10JVMWuC8tp1WlnGmhOagBCvP0adDdxfD0zh_3wwuGeh77SGMqaGKKCk4o_X_UaEkJTO-R8kBNTGkFKFrdtENOk4NJc1-wuZ1wuY44ax8PNbHdgD7V3jdrPwDvXybpg</recordid><startdate>20141015</startdate><enddate>20141015</enddate><creator>Xu, Xuan</creator><creator>Qiu, Chao</creator><creator>Zhu, Lingyan</creator><creator>Huang, Jun</creator><creator>Li, Lishuang</creator><creator>Fu, Weihui</creator><creator>Zhang, Linxia</creator><creator>Wei, Jun</creator><creator>Wang, Ying</creator><creator>Geng, Yunqi</creator><creator>Zhang, Xiaoyan</creator><creator>Qiao, Wentao</creator><creator>Xu, Jianqing</creator><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>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20141015</creationdate><title>IFN-stimulated gene LY6E in monocytes regulates the CD14/TLR4 pathway but inadequately restrains the hyperactivation of monocytes during chronic HIV-1 infection</title><author>Xu, Xuan ; 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Albeit most ISGs are important effectors for containing viral replication, some might exert compensatory immune suppression to limit pathological dysfunctions, although the mechanisms are not fully understood. In this study, we report that the ISG lymphocyte Ag 6 complex, locus E (LY6E) is a negative immune regulator of monocytes. LY6E in monocytes negatively modulated CD14 expression and subsequently dampened the responsiveness to LPS stimulation in vitro. In the setting of chronic HIV infection, the upregulation of LY6E was correlated with reduced CD14 level on monocytes; however, the immunosuppressive effect of LY6E was not adequate to remedy the hyperresponsiveness of activated monocytes. Taken together, the regulatory LY6E pathway in monocytes represents one of negative feedback mechanisms that counterbalance monocyte activation, which might be caused by LPS translocation through the compromised gastrointestinal tract during persistent HIV-1 infection and may serve as a potential target for immune intervention.</abstract><cop>United States</cop><pmid>25225669</pmid><doi>10.4049/jimmunol.1401249</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Antigens, Surface - genetics Antigens, Surface - immunology Cell Line, Tumor Female Gastrointestinal Tract - immunology GPI-Linked Proteins - genetics GPI-Linked Proteins - immunology HeLa Cells HIV Infections - immunology HIV Infections - virology HIV-1 - immunology Human immunodeficiency virus Human immunodeficiency virus 1 Humans Immune Tolerance Interferon Regulatory Factors - genetics Interferon-alpha - immunology Interferon-alpha - pharmacology Lentivirus Lipopolysaccharide Receptors - biosynthesis Lipopolysaccharide Receptors - immunology Lipopolysaccharides - immunology Male Middle Aged Monocytes - immunology RNA Interference RNA, Small Interfering Signal Transduction - immunology Toll-Like Receptor 4 - immunology Tumor Necrosis Factor-alpha - biosynthesis Up-Regulation Virus Replication - immunology |
| title | IFN-stimulated gene LY6E in monocytes regulates the CD14/TLR4 pathway but inadequately restrains the hyperactivation of monocytes during chronic HIV-1 infection |
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