IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis

Abstract Myeloid cells, key players in atherosclerosis, take up and present antigens, leading to systemic and local T cell activation. The recruitment and activation of immune cells to the aorta in atherosclerosis is regulated by adhesion molecules, chemokines and cytokines. IL-27R is an immunoregul...

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Autores principales:	Iuliia O. Peshkova, Aliia R. Fatkhullina, Zbigniew Mikulski, Klaus Ley, Ekaterina K. Koltsova
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/877dc4435eed4f7b9c280442a25a03ee
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spelling	oai:doaj.org-article:877dc4435eed4f7b9c280442a25a03ee2021-12-02T16:07:58ZIL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis10.1038/s41598-017-01828-82045-2322https://doaj.org/article/877dc4435eed4f7b9c280442a25a03ee2017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01828-8https://doaj.org/toc/2045-2322Abstract Myeloid cells, key players in atherosclerosis, take up and present antigens, leading to systemic and local T cell activation. The recruitment and activation of immune cells to the aorta in atherosclerosis is regulated by adhesion molecules, chemokines and cytokines. IL-27R is an immunoregulatory signaling nod in autoimmune and infectious pathologies. IL-27R was shown to suppress T cells activation in atherosclerosis, however it’s possible role in myeloid cell accumulation and activation is not understood. Here we demonstrate that Apoe −/− Il27ra −/− mice fed with “Western Diet” for 7 or 18 weeks developed significantly more atherosclerosis compared to Apoe −/− Il27ra +/− controls. Accelerated disease was driven by enhanced expression of adhesion molecules and chemokines causing the accumulation of immune cells. Myeloid cells produced more inflammatory cytokines and upregulated MHCII. Multiphoton microscopy revealed more efficient interactions between aortic myeloid cells and CD4+ T cells. Overall, we show that IL-27R signaling controls endothelial cells activation and myeloid cell recruitment at early and advanced stages of atherosclerosis. In the absence of IL-27R myeloid cells become hyperactivated, produce pro-inflammatory cytokines and act as more potent antigen presenting cells. Enhanced interactions between Il27ra −/− APC and CD4+ T cells in the aortic wall contribute to T cells re-activation and pro-atherogenic cytokine production.Iuliia O. PeshkovaAliia R. FatkhullinaZbigniew MikulskiKlaus LeyEkaterina K. KoltsovaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Iuliia O. Peshkova Aliia R. Fatkhullina Zbigniew Mikulski Klaus Ley Ekaterina K. Koltsova IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
description	Abstract Myeloid cells, key players in atherosclerosis, take up and present antigens, leading to systemic and local T cell activation. The recruitment and activation of immune cells to the aorta in atherosclerosis is regulated by adhesion molecules, chemokines and cytokines. IL-27R is an immunoregulatory signaling nod in autoimmune and infectious pathologies. IL-27R was shown to suppress T cells activation in atherosclerosis, however it’s possible role in myeloid cell accumulation and activation is not understood. Here we demonstrate that Apoe −/− Il27ra −/− mice fed with “Western Diet” for 7 or 18 weeks developed significantly more atherosclerosis compared to Apoe −/− Il27ra +/− controls. Accelerated disease was driven by enhanced expression of adhesion molecules and chemokines causing the accumulation of immune cells. Myeloid cells produced more inflammatory cytokines and upregulated MHCII. Multiphoton microscopy revealed more efficient interactions between aortic myeloid cells and CD4+ T cells. Overall, we show that IL-27R signaling controls endothelial cells activation and myeloid cell recruitment at early and advanced stages of atherosclerosis. In the absence of IL-27R myeloid cells become hyperactivated, produce pro-inflammatory cytokines and act as more potent antigen presenting cells. Enhanced interactions between Il27ra −/− APC and CD4+ T cells in the aortic wall contribute to T cells re-activation and pro-atherogenic cytokine production.
format	article
author	Iuliia O. Peshkova Aliia R. Fatkhullina Zbigniew Mikulski Klaus Ley Ekaterina K. Koltsova
author_facet	Iuliia O. Peshkova Aliia R. Fatkhullina Zbigniew Mikulski Klaus Ley Ekaterina K. Koltsova
author_sort	Iuliia O. Peshkova
title	IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
title_short	IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
title_full	IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
title_fullStr	IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
title_full_unstemmed	IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
title_sort	il-27r signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/877dc4435eed4f7b9c280442a25a03ee
work_keys_str_mv	AT iuliiaopeshkova il27rsignalingcontrolsmyeloidcellsaccumulationandantigenpresentationinatherosclerosis AT aliiarfatkhullina il27rsignalingcontrolsmyeloidcellsaccumulationandantigenpresentationinatherosclerosis AT zbigniewmikulski il27rsignalingcontrolsmyeloidcellsaccumulationandantigenpresentationinatherosclerosis AT klausley il27rsignalingcontrolsmyeloidcellsaccumulationandantigenpresentationinatherosclerosis AT ekaterinakkoltsova il27rsignalingcontrolsmyeloidcellsaccumulationandantigenpresentationinatherosclerosis
_version_	1718384669456596992

IL-27R signaling controls myeloid cells accumulation and antigen-presentation in atherosclerosis

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