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

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...

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Autores principales: Liao, Chia‐Te, Rosas, Marcela, Davies, Luke C., Giles, Peter J., Tyrrell, Victoria J., O'Donnell, Valerie B., Topley, Nicholas, Humphreys, Ian R., Fraser, Donald J., Jones, Simon A., Taylor, Philip R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5026061/
https://www.ncbi.nlm.nih.gov/pubmed/27378515
http://dx.doi.org/10.1002/eji.201646528
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author Liao, Chia‐Te
Rosas, Marcela
Davies, Luke C.
Giles, Peter J.
Tyrrell, Victoria J.
O'Donnell, Valerie B.
Topley, Nicholas
Humphreys, Ian R.
Fraser, Donald J.
Jones, Simon A.
Taylor, Philip R.
author_facet Liao, Chia‐Te
Rosas, Marcela
Davies, Luke C.
Giles, Peter J.
Tyrrell, Victoria J.
O'Donnell, Valerie B.
Topley, Nicholas
Humphreys, Ian R.
Fraser, Donald J.
Jones, Simon A.
Taylor, Philip R.
author_sort Liao, Chia‐Te
collection PubMed
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.
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spelling pubmed-50260612016-10-03 IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation Liao, Chia‐Te Rosas, Marcela Davies, Luke C. Giles, Peter J. Tyrrell, Victoria J. O'Donnell, Valerie B. Topley, Nicholas Humphreys, Ian R. Fraser, Donald J. Jones, Simon A. Taylor, Philip R. Eur J Immunol Allergy and inflammation 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. John Wiley and Sons Inc. 2016-07-28 2016-09 /pmc/articles/PMC5026061/ /pubmed/27378515 http://dx.doi.org/10.1002/eji.201646528 Text en © 2016 The Authors. European Journal of Immunology published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Allergy and inflammation
Liao, Chia‐Te
Rosas, Marcela
Davies, Luke C.
Giles, Peter J.
Tyrrell, Victoria J.
O'Donnell, Valerie B.
Topley, Nicholas
Humphreys, Ian R.
Fraser, Donald J.
Jones, Simon A.
Taylor, Philip R.
IL‐10 differentially controls the infiltration of inflammatory macrophages and antigen‐presenting cells during inflammation
title 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_short 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
topic Allergy and inflammation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5026061/
https://www.ncbi.nlm.nih.gov/pubmed/27378515
http://dx.doi.org/10.1002/eji.201646528
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