Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses

Abstract Interleukin-36 (IL-36) represents three cytokines, IL-36α, IL-36β and IL-36γ, which bind to the same receptor, IL-1RL2; however, their physiological function(s) remain poorly understood. Here, the role of IL-36 in immunity against HSV-1 was examined using the flank skin infection mouse mode...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Katelynn A. Milora, Siva R. Uppalapati, Julio C. Sanmiguel, Wei Zou, Liselotte E. Jensen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7b7a12157bfa4f488dd7a6d2de90cae1
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:7b7a12157bfa4f488dd7a6d2de90cae1
record_format	dspace
spelling	oai:doaj.org-article:7b7a12157bfa4f488dd7a6d2de90cae12021-12-02T12:30:18ZInterleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses10.1038/s41598-017-05363-42045-2322https://doaj.org/article/7b7a12157bfa4f488dd7a6d2de90cae12017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05363-4https://doaj.org/toc/2045-2322Abstract Interleukin-36 (IL-36) represents three cytokines, IL-36α, IL-36β and IL-36γ, which bind to the same receptor, IL-1RL2; however, their physiological function(s) remain poorly understood. Here, the role of IL-36 in immunity against HSV-1 was examined using the flank skin infection mouse model. Expression analyses revealed increased levels of IL-36α and IL-36β mRNA in infected skin, while constitutive IL-36γ levels remained largely unchanged. In human keratinocytes, IL-36α mRNA was induced by HSV-1, while IL-1β and TNFα increased all three IL-36 mRNAs. The dominant alternative splice variant of human IL-36β mRNA was isoform 2, which is the ortholog of the known mouse IL-36β mRNA. Mice deficient in IL-36β, but not IL-36α or IL-36γ, succumbed more frequently to HSV-1 infection than wild type mice. Furthermore, IL-36β−/− mice developed larger zosteriform skin lesions along infected neurons. Levels of HSV-1 specific antibodies, CD8+ cells and IFNγ-producing CD4+ cells were statistically equal in wild type and IL-36β−/− mice, suggesting similar initiation of adaptive immunity in the two strains. This correlated with the time at which HSV-1 genome and mRNA levels in primary skin lesions started to decline in both wild type and IL-36β−/− mice. Our data indicate that IL-36β has previously unrecognized functions protective against HSV-1 infection.Katelynn A. MiloraSiva R. UppalapatiJulio C. SanmiguelWei ZouLiselotte E. JensenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-16 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Katelynn A. Milora Siva R. Uppalapati Julio C. Sanmiguel Wei Zou Liselotte E. Jensen Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
description	Abstract Interleukin-36 (IL-36) represents three cytokines, IL-36α, IL-36β and IL-36γ, which bind to the same receptor, IL-1RL2; however, their physiological function(s) remain poorly understood. Here, the role of IL-36 in immunity against HSV-1 was examined using the flank skin infection mouse model. Expression analyses revealed increased levels of IL-36α and IL-36β mRNA in infected skin, while constitutive IL-36γ levels remained largely unchanged. In human keratinocytes, IL-36α mRNA was induced by HSV-1, while IL-1β and TNFα increased all three IL-36 mRNAs. The dominant alternative splice variant of human IL-36β mRNA was isoform 2, which is the ortholog of the known mouse IL-36β mRNA. Mice deficient in IL-36β, but not IL-36α or IL-36γ, succumbed more frequently to HSV-1 infection than wild type mice. Furthermore, IL-36β−/− mice developed larger zosteriform skin lesions along infected neurons. Levels of HSV-1 specific antibodies, CD8+ cells and IFNγ-producing CD4+ cells were statistically equal in wild type and IL-36β−/− mice, suggesting similar initiation of adaptive immunity in the two strains. This correlated with the time at which HSV-1 genome and mRNA levels in primary skin lesions started to decline in both wild type and IL-36β−/− mice. Our data indicate that IL-36β has previously unrecognized functions protective against HSV-1 infection.
format	article
author	Katelynn A. Milora Siva R. Uppalapati Julio C. Sanmiguel Wei Zou Liselotte E. Jensen
author_facet	Katelynn A. Milora Siva R. Uppalapati Julio C. Sanmiguel Wei Zou Liselotte E. Jensen
author_sort	Katelynn A. Milora
title	Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
title_short	Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
title_full	Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
title_fullStr	Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
title_full_unstemmed	Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
title_sort	interleukin-36β provides protection against hsv-1 infection, but does not modulate initiation of adaptive immune responses
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/7b7a12157bfa4f488dd7a6d2de90cae1
work_keys_str_mv	AT katelynnamilora interleukin36bprovidesprotectionagainsthsv1infectionbutdoesnotmodulateinitiationofadaptiveimmuneresponses AT sivaruppalapati interleukin36bprovidesprotectionagainsthsv1infectionbutdoesnotmodulateinitiationofadaptiveimmuneresponses AT juliocsanmiguel interleukin36bprovidesprotectionagainsthsv1infectionbutdoesnotmodulateinitiationofadaptiveimmuneresponses AT weizou interleukin36bprovidesprotectionagainsthsv1infectionbutdoesnotmodulateinitiationofadaptiveimmuneresponses AT liselotteejensen interleukin36bprovidesprotectionagainsthsv1infectionbutdoesnotmodulateinitiationofadaptiveimmuneresponses
_version_	1718394404996120576

Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses

Ejemplares similares