Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection

Abstract Viral infections of the cornea including herpes simplex virus 1 (HSV-1) cause visual morbidity, and the corneal endothelial cell damage leads to significant visual impairment. Interferon regulatory factor 7 (IRF7) has been identified as a significant regulator in corneal endothelial cells a...

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Autores principales:	Fumie Ohtani, Dai Miyazaki, Yumiko Shimizu, Tomoko Haruki, Satoru Yamagami, Yoshitsugu Inoue
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d525e5f2a6074af79da33093be0a70dc
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spelling	oai:doaj.org-article:d525e5f2a6074af79da33093be0a70dc2021-12-02T18:50:59ZRole of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection10.1038/s41598-021-95823-92045-2322https://doaj.org/article/d525e5f2a6074af79da33093be0a70dc2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-95823-9https://doaj.org/toc/2045-2322Abstract Viral infections of the cornea including herpes simplex virus 1 (HSV-1) cause visual morbidity, and the corneal endothelial cell damage leads to significant visual impairment. Interferon regulatory factor 7 (IRF7) has been identified as a significant regulator in corneal endothelial cells after an HSV-1 infection. To examine the role played by IRF7, the DNA binding domain (DBD) of IRF7 of human corneal endothelial cells (HCEn) was disrupted. An RNAi inhibition of IRF7 and IRF7 DBD disruption (IRF7 ∆DBD) led to an impairment of IFN-β production. Impaired IFN-β production by IRF7 ∆DBD was regained by IRF7 DNA transfection. Transcriptional network analysis indicated that IRF7 plays a role in antigen presentation function of corneal endothelial cells. When the antigen presentation activity of HCEn cells were examined for priming of memory CD8 T cells, IRF7 disruption abolished the anti-viral cytotoxic T lymphocyte (CTL) response which was dependent on the major histocompatibility complex (MHC) class I. To further examine the roles played by IRF7 in CTL induction as acquired immunity, the contribution of IRF7 to MHC class I-mediated antigen presentation was assessed. Analysis of IRF7 ∆DBD cells indicated that IRF7 played an unrecognized role in MHC class I induction, and the viral infection induced-MHC class I induction was abolished by IRF7 disruption. Collectively, the IRF7 in corneal endothelial cells not only contributed to type I IFN response, but also to the mediation of viral infection-induced MHC class I upregulation and priming of CD8 arm of acquired immunity.Fumie OhtaniDai MiyazakiYumiko ShimizuTomoko HarukiSatoru YamagamiYoshitsugu InoueNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Fumie Ohtani Dai Miyazaki Yumiko Shimizu Tomoko Haruki Satoru Yamagami Yoshitsugu Inoue Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection
description	Abstract Viral infections of the cornea including herpes simplex virus 1 (HSV-1) cause visual morbidity, and the corneal endothelial cell damage leads to significant visual impairment. Interferon regulatory factor 7 (IRF7) has been identified as a significant regulator in corneal endothelial cells after an HSV-1 infection. To examine the role played by IRF7, the DNA binding domain (DBD) of IRF7 of human corneal endothelial cells (HCEn) was disrupted. An RNAi inhibition of IRF7 and IRF7 DBD disruption (IRF7 ∆DBD) led to an impairment of IFN-β production. Impaired IFN-β production by IRF7 ∆DBD was regained by IRF7 DNA transfection. Transcriptional network analysis indicated that IRF7 plays a role in antigen presentation function of corneal endothelial cells. When the antigen presentation activity of HCEn cells were examined for priming of memory CD8 T cells, IRF7 disruption abolished the anti-viral cytotoxic T lymphocyte (CTL) response which was dependent on the major histocompatibility complex (MHC) class I. To further examine the roles played by IRF7 in CTL induction as acquired immunity, the contribution of IRF7 to MHC class I-mediated antigen presentation was assessed. Analysis of IRF7 ∆DBD cells indicated that IRF7 played an unrecognized role in MHC class I induction, and the viral infection induced-MHC class I induction was abolished by IRF7 disruption. Collectively, the IRF7 in corneal endothelial cells not only contributed to type I IFN response, but also to the mediation of viral infection-induced MHC class I upregulation and priming of CD8 arm of acquired immunity.
format	article
author	Fumie Ohtani Dai Miyazaki Yumiko Shimizu Tomoko Haruki Satoru Yamagami Yoshitsugu Inoue
author_facet	Fumie Ohtani Dai Miyazaki Yumiko Shimizu Tomoko Haruki Satoru Yamagami Yoshitsugu Inoue
author_sort	Fumie Ohtani
title	Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection
title_short	Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection
title_full	Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection
title_fullStr	Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection
title_full_unstemmed	Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection
title_sort	role of interferon regulatory factor 7 in corneal endothelial cells after hsv-1 infection
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/d525e5f2a6074af79da33093be0a70dc
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Role of interferon regulatory factor 7 in corneal endothelial cells after HSV-1 infection

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