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Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors

BACKGROUND: Monocytes and macrophages produce interleukin (IL)-10, an immunoregulatory cytokine and a potent therapeutic tool for immune disorders. Augmentation of IL-10 production with a concomitant reduction of proinflammatory cytokines in macrophages in vitro is attained by doubly stimulating the...

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Autores principales: Inui, Masanori, Tazawa, Kino, Kishi, Yoshiro, Takai, Toshiyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407389/
https://www.ncbi.nlm.nih.gov/pubmed/25896516
http://dx.doi.org/10.1186/s12865-015-0086-z
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author Inui, Masanori
Tazawa, Kino
Kishi, Yoshiro
Takai, Toshiyuki
author_facet Inui, Masanori
Tazawa, Kino
Kishi, Yoshiro
Takai, Toshiyuki
author_sort Inui, Masanori
collection PubMed
description BACKGROUND: Monocytes and macrophages produce interleukin (IL)-10, an immunoregulatory cytokine and a potent therapeutic tool for immune disorders. Augmentation of IL-10 production with a concomitant reduction of proinflammatory cytokines in macrophages in vitro is attained by doubly stimulating the cells with a toll-like receptor ligand and immunoglobulin (Ig)G immune complexes, a response known as that of regulatory (or alternatively activated/M2) macrophages. However, it has not been explored sufficiently how such a regulatory response could be exploited for anti-inflammation. Our objective is to find a potential way or condition for augmenting IL-10 by monocytes/macrophages in vivo and in vitro. RESULTS: We show that platelets, when they are opsonized with IgG, can convert human peripheral blood circulating monocytes to IL-10-producing regulatory monocytes in vitro and also in a murine in vivo model. Co-culturing of platelets and monocytes in the presence of anti-integrin IgG and a bacterial lipopolysaccharide augmented IL-10 production via a direct interaction between platelets and monocytes. This novel way of enhancing IL-10 was mediated by activating-type Fc receptors for IgG. CONCLUSION: These findings indicate that the IgG-bound platelet-induced conversion of monocytes to regulatory cells might provide a novel strategy for controlling inflammation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12865-015-0086-z) contains supplementary material, which is available to authorized users.
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spelling pubmed-44073892015-04-24 Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors Inui, Masanori Tazawa, Kino Kishi, Yoshiro Takai, Toshiyuki BMC Immunol Research Article BACKGROUND: Monocytes and macrophages produce interleukin (IL)-10, an immunoregulatory cytokine and a potent therapeutic tool for immune disorders. Augmentation of IL-10 production with a concomitant reduction of proinflammatory cytokines in macrophages in vitro is attained by doubly stimulating the cells with a toll-like receptor ligand and immunoglobulin (Ig)G immune complexes, a response known as that of regulatory (or alternatively activated/M2) macrophages. However, it has not been explored sufficiently how such a regulatory response could be exploited for anti-inflammation. Our objective is to find a potential way or condition for augmenting IL-10 by monocytes/macrophages in vivo and in vitro. RESULTS: We show that platelets, when they are opsonized with IgG, can convert human peripheral blood circulating monocytes to IL-10-producing regulatory monocytes in vitro and also in a murine in vivo model. Co-culturing of platelets and monocytes in the presence of anti-integrin IgG and a bacterial lipopolysaccharide augmented IL-10 production via a direct interaction between platelets and monocytes. This novel way of enhancing IL-10 was mediated by activating-type Fc receptors for IgG. CONCLUSION: These findings indicate that the IgG-bound platelet-induced conversion of monocytes to regulatory cells might provide a novel strategy for controlling inflammation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12865-015-0086-z) contains supplementary material, which is available to authorized users. BioMed Central 2015-04-21 /pmc/articles/PMC4407389/ /pubmed/25896516 http://dx.doi.org/10.1186/s12865-015-0086-z Text en © Inui et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Inui, Masanori
Tazawa, Kino
Kishi, Yoshiro
Takai, Toshiyuki
Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
title Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
title_full Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
title_fullStr Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
title_full_unstemmed Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
title_short Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors
title_sort platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin g and activating-type fcγ receptors
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407389/
https://www.ncbi.nlm.nih.gov/pubmed/25896516
http://dx.doi.org/10.1186/s12865-015-0086-z
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