Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway

Abstract Interleukin-27 (IL-27) is a cytokine that suppresses human immunodeficiency virus (HIV)-1 infection in macrophages and is considered as an immunotherapeutic reagent for infectious diseases. It is reported that IL-27 suppresses autophagy in Mycobacterium tuberculosis-infected macrophages; ho...

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Autores principales:	Sylvain Laverdure, Ziqiu Wang, Jun Yang, Takuya Yamamoto, Tima Thomas, Toyotaka Sato, Kunio Nagashima, Tomozumi Imamichi
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/55569853dea542f185d3d806065218a4
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spelling	oai:doaj.org-article:55569853dea542f185d3d806065218a42021-12-02T16:26:23ZInterleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway10.1038/s41598-021-94061-32045-2322https://doaj.org/article/55569853dea542f185d3d806065218a42021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94061-3https://doaj.org/toc/2045-2322Abstract Interleukin-27 (IL-27) is a cytokine that suppresses human immunodeficiency virus (HIV)-1 infection in macrophages and is considered as an immunotherapeutic reagent for infectious diseases. It is reported that IL-27 suppresses autophagy in Mycobacterium tuberculosis-infected macrophages; however, a role for IL-27 on autophagy induction has been less studied. In this study, we investigated the impact of IL-27 in both autophagy induction and HIV-1 infection in macrophages. Primary human monocytes were differentiated into macrophages using human AB serum (huAB) alone, macrophage-colony stimulating factor (M-CSF) alone, or a combination of IL-27 with huAB or M-CSF. Electron microscopy and immunofluorescence staining demonstrated that a 20-fold increase in autophagosome formation was only detected in IL-27 + huAB-induced macrophages. Western blot analysis indicated that the autophagosome induction was not linked to either dephosphorylation of the mammalian target of rapamycin (mTOR) or lipidation of microtubule-associated protein 1A/1B-light chain 3 (LC3), an autophagosomal marker, implying that IL-27 can induce autophagy through a novel non-canonical pathway. Here we show for the first time that IL-27 induces autophagy during monocyte-to-macrophage differentiation in a subtype-dependent manner.Sylvain LaverdureZiqiu WangJun YangTakuya YamamotoTima ThomasToyotaka SatoKunio NagashimaTomozumi ImamichiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sylvain Laverdure Ziqiu Wang Jun Yang Takuya Yamamoto Tima Thomas Toyotaka Sato Kunio Nagashima Tomozumi Imamichi Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway
description	Abstract Interleukin-27 (IL-27) is a cytokine that suppresses human immunodeficiency virus (HIV)-1 infection in macrophages and is considered as an immunotherapeutic reagent for infectious diseases. It is reported that IL-27 suppresses autophagy in Mycobacterium tuberculosis-infected macrophages; however, a role for IL-27 on autophagy induction has been less studied. In this study, we investigated the impact of IL-27 in both autophagy induction and HIV-1 infection in macrophages. Primary human monocytes were differentiated into macrophages using human AB serum (huAB) alone, macrophage-colony stimulating factor (M-CSF) alone, or a combination of IL-27 with huAB or M-CSF. Electron microscopy and immunofluorescence staining demonstrated that a 20-fold increase in autophagosome formation was only detected in IL-27 + huAB-induced macrophages. Western blot analysis indicated that the autophagosome induction was not linked to either dephosphorylation of the mammalian target of rapamycin (mTOR) or lipidation of microtubule-associated protein 1A/1B-light chain 3 (LC3), an autophagosomal marker, implying that IL-27 can induce autophagy through a novel non-canonical pathway. Here we show for the first time that IL-27 induces autophagy during monocyte-to-macrophage differentiation in a subtype-dependent manner.
format	article
author	Sylvain Laverdure Ziqiu Wang Jun Yang Takuya Yamamoto Tima Thomas Toyotaka Sato Kunio Nagashima Tomozumi Imamichi
author_facet	Sylvain Laverdure Ziqiu Wang Jun Yang Takuya Yamamoto Tima Thomas Toyotaka Sato Kunio Nagashima Tomozumi Imamichi
author_sort	Sylvain Laverdure
title	Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway
title_short	Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway
title_full	Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway
title_fullStr	Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway
title_full_unstemmed	Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway
title_sort	interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mtor- and lc3-independent pathway
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/55569853dea542f185d3d806065218a4
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Interleukin-27 promotes autophagy in human serum-induced primary macrophages via an mTOR- and LC3-independent pathway

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