No Cover Image

Journal article 817 views 64 downloads

IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation

Chia‐Te Liao, Marcela Rosas, Luke Davies Orcid Logo, Peter J. Giles, Victoria J. Tyrrell, Valerie B. O'Donnell, Nicholas Topley, Ian R. Humphreys, Donald J. Fraser, Simon A. Jones, Philip R. Taylor

European Journal of Immunology, Volume: 46, Issue: 9, Pages: 2222 - 2232

Swansea University Author: Luke Davies Orcid Logo

  • 61705.pdf

    PDF | Version of Record

    Copyright 2016 The Authors. This is an open access article under the terms of the Creative Commons Attribution License

    Download (2.09MB)

Check full text

DOI (Published version): 10.1002/eji.201646528

Abstract

The inflammatory activation and recruitment of defined myeloid populations is essential for controlling the bridge between innate and adaptive immunity and shaping the immune response to microbial challenge. However, these cells exhibit significant functional heterogeneity and the inflammatory signa...

Full description

Published in: European Journal of Immunology
ISSN: 0014-2980 1521-4141
Published: Wiley 2016
Online Access: Check full text

URI: https://cronfa.swan.ac.uk/Record/cronfa61705
Tags: Add Tag
No Tags, Be the first to tag this record!
first_indexed 2022-11-07T11:03:36Z
last_indexed 2023-01-13T19:22:38Z
id cronfa61705
recordtype SURis
fullrecord <?xml version="1.0"?><rfc1807><datestamp>2022-11-07T11:05:33.1827876</datestamp><bib-version>v2</bib-version><id>61705</id><entry>2022-10-31</entry><title>IL&#x2010;10 differentially controls the infiltration of inflammatory macrophages and antigen&#x2010;presenting cells during inflammation</title><swanseaauthors><author><sid>ff080296775381560053d5e3a6e81745</sid><ORCID>0000-0001-7767-4060</ORCID><firstname>Luke</firstname><surname>Davies</surname><name>Luke Davies</name><active>true</active><ethesisStudent>false</ethesisStudent></author></swanseaauthors><date>2022-10-31</date><deptcode>BMS</deptcode><abstract>The inflammatory activation and recruitment of defined myeloid populations is essential for controlling the bridge between innate and adaptive immunity and shaping the immune response to microbial challenge. However, these cells exhibit significant functional heterogeneity and the inflammatory signals that differentially influence their effector characteristics are poorly characterized. In this study, we defined the phenotype of discrete subsets of effective antigen-presenting cells (APCs) in the peritoneal cavity during peritonitis. When the functional properties of these cells were compared to inflammatory monocyte-derived macrophages we noted differential responses to the immune-modulatory cytokine IL-10. In contrast to the suppressive actions of IL-10 on inflammatory macrophages, the recruitment of APCs was relatively refractory and we found no evidence for selective inhibition of APC differentiation. This differential response of myeloid cell subsets to IL-10 may thus have limited impact on development of potentially tissue-damaging adaptive immune responses, while restricting the magnitude of the inflammatory response. These findings may have clinical relevance in the context of peritoneal dialysis patients, where recurrent infections are associated with immune-mediated membrane dysfunction, treatment failure, and increased morbidity.</abstract><type>Journal Article</type><journal>European Journal of Immunology</journal><volume>46</volume><journalNumber>9</journalNumber><paginationStart>2222</paginationStart><paginationEnd>2232</paginationEnd><publisher>Wiley</publisher><placeOfPublication/><isbnPrint/><isbnElectronic/><issnPrint>0014-2980</issnPrint><issnElectronic>1521-4141</issnElectronic><keywords>Antigen presenting; Antigen processing; Dendritic cells; Fate-mapping; Inflammation; Macrophages; Monocytes</keywords><publishedDay>7</publishedDay><publishedMonth>9</publishedMonth><publishedYear>2016</publishedYear><publishedDate>2016-09-07</publishedDate><doi>10.1002/eji.201646528</doi><url/><notes/><college>COLLEGE NANME</college><department>Biomedical Sciences</department><CollegeCode>COLLEGE CODE</CollegeCode><DepartmentCode>BMS</DepartmentCode><institution>Swansea University</institution><apcterm/><funders>Wellcome Trust. Grant Numbers: 094143/Z/10/Z, WT107964MA; Medical Research Council. Grant Numbers: G0601617/1, MR/K02003X1</funders><projectreference/><lastEdited>2022-11-07T11:05:33.1827876</lastEdited><Created>2022-10-31T12:40:23.2092409</Created><path><level id="1">Faculty of Medicine, Health and Life Sciences</level><level id="2">Swansea University Medical School - Medicine</level></path><authors><author><firstname>Chia&#x2010;Te</firstname><surname>Liao</surname><order>1</order></author><author><firstname>Marcela</firstname><surname>Rosas</surname><order>2</order></author><author><firstname>Luke</firstname><surname>Davies</surname><orcid>0000-0001-7767-4060</orcid><order>3</order></author><author><firstname>Peter J.</firstname><surname>Giles</surname><order>4</order></author><author><firstname>Victoria J.</firstname><surname>Tyrrell</surname><order>5</order></author><author><firstname>Valerie B.</firstname><surname>O'Donnell</surname><order>6</order></author><author><firstname>Nicholas</firstname><surname>Topley</surname><order>7</order></author><author><firstname>Ian R.</firstname><surname>Humphreys</surname><order>8</order></author><author><firstname>Donald J.</firstname><surname>Fraser</surname><order>9</order></author><author><firstname>Simon A.</firstname><surname>Jones</surname><order>10</order></author><author><firstname>Philip R.</firstname><surname>Taylor</surname><order>11</order></author></authors><documents><document><filename>61705__25664__470f59e7120f4750b9102b8894878979.pdf</filename><originalFilename>61705.pdf</originalFilename><uploaded>2022-11-07T11:04:08.6745596</uploaded><type>Output</type><contentLength>2193353</contentLength><contentType>application/pdf</contentType><version>Version of Record</version><cronfaStatus>true</cronfaStatus><documentNotes>Copyright 2016 The Authors. This is an open access article under the terms of the Creative Commons Attribution License</documentNotes><copyrightCorrect>true</copyrightCorrect><language>eng</language><licence>http://creativecommons.org/licenses/by/4.0/</licence></document></documents><OutputDurs/></rfc1807>
spelling 2022-11-07T11:05:33.1827876 v2 61705 2022-10-31 IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation ff080296775381560053d5e3a6e81745 0000-0001-7767-4060 Luke Davies Luke Davies true false 2022-10-31 BMS The inflammatory activation and recruitment of defined myeloid populations is essential for controlling the bridge between innate and adaptive immunity and shaping the immune response to microbial challenge. However, these cells exhibit significant functional heterogeneity and the inflammatory signals that differentially influence their effector characteristics are poorly characterized. In this study, we defined the phenotype of discrete subsets of effective antigen-presenting cells (APCs) in the peritoneal cavity during peritonitis. When the functional properties of these cells were compared to inflammatory monocyte-derived macrophages we noted differential responses to the immune-modulatory cytokine IL-10. In contrast to the suppressive actions of IL-10 on inflammatory macrophages, the recruitment of APCs was relatively refractory and we found no evidence for selective inhibition of APC differentiation. This differential response of myeloid cell subsets to IL-10 may thus have limited impact on development of potentially tissue-damaging adaptive immune responses, while restricting the magnitude of the inflammatory response. These findings may have clinical relevance in the context of peritoneal dialysis patients, where recurrent infections are associated with immune-mediated membrane dysfunction, treatment failure, and increased morbidity. Journal Article European Journal of Immunology 46 9 2222 2232 Wiley 0014-2980 1521-4141 Antigen presenting; Antigen processing; Dendritic cells; Fate-mapping; Inflammation; Macrophages; Monocytes 7 9 2016 2016-09-07 10.1002/eji.201646528 COLLEGE NANME Biomedical Sciences COLLEGE CODE BMS Swansea University Wellcome Trust. Grant Numbers: 094143/Z/10/Z, WT107964MA; Medical Research Council. Grant Numbers: G0601617/1, MR/K02003X1 2022-11-07T11:05:33.1827876 2022-10-31T12:40:23.2092409 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine Chia‐Te Liao 1 Marcela Rosas 2 Luke Davies 0000-0001-7767-4060 3 Peter J. Giles 4 Victoria J. Tyrrell 5 Valerie B. O'Donnell 6 Nicholas Topley 7 Ian R. Humphreys 8 Donald J. Fraser 9 Simon A. Jones 10 Philip R. Taylor 11 61705__25664__470f59e7120f4750b9102b8894878979.pdf 61705.pdf 2022-11-07T11:04:08.6745596 Output 2193353 application/pdf Version of Record true Copyright 2016 The Authors. This is an open access article under the terms of the Creative Commons Attribution License true eng http://creativecommons.org/licenses/by/4.0/
title IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
spellingShingle IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
Luke Davies
title_short IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
title_full IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
title_fullStr IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
title_full_unstemmed IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
title_sort IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
author_id_str_mv ff080296775381560053d5e3a6e81745
author_id_fullname_str_mv ff080296775381560053d5e3a6e81745_***_Luke Davies
author Luke Davies
author2 Chia‐Te Liao
Marcela Rosas
Luke Davies
Peter J. Giles
Victoria J. Tyrrell
Valerie B. O'Donnell
Nicholas Topley
Ian R. Humphreys
Donald J. Fraser
Simon A. Jones
Philip R. Taylor
format Journal article
container_title European Journal of Immunology
container_volume 46
container_issue 9
container_start_page 2222
publishDate 2016
institution Swansea University
issn 0014-2980
1521-4141
doi_str_mv 10.1002/eji.201646528
publisher Wiley
college_str Faculty of Medicine, Health and Life Sciences
hierarchytype
hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
document_store_str 1
active_str 0
description The inflammatory activation and recruitment of defined myeloid populations is essential for controlling the bridge between innate and adaptive immunity and shaping the immune response to microbial challenge. However, these cells exhibit significant functional heterogeneity and the inflammatory signals that differentially influence their effector characteristics are poorly characterized. In this study, we defined the phenotype of discrete subsets of effective antigen-presenting cells (APCs) in the peritoneal cavity during peritonitis. When the functional properties of these cells were compared to inflammatory monocyte-derived macrophages we noted differential responses to the immune-modulatory cytokine IL-10. In contrast to the suppressive actions of IL-10 on inflammatory macrophages, the recruitment of APCs was relatively refractory and we found no evidence for selective inhibition of APC differentiation. This differential response of myeloid cell subsets to IL-10 may thus have limited impact on development of potentially tissue-damaging adaptive immune responses, while restricting the magnitude of the inflammatory response. These findings may have clinical relevance in the context of peritoneal dialysis patients, where recurrent infections are associated with immune-mediated membrane dysfunction, treatment failure, and increased morbidity.
published_date 2016-09-07T04:20:43Z
_version_ 1763754370613116928
score 11.037581