About: Differential expression of interferon-lambda receptor 1 splice variants determines the magnitude of the antiviral response induced by interferon-lambda 3 in human immune cells

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Differential expression of interferon-lambda receptor 1 splice variants determines the magnitude of the antiviral response induced by interferon-lambda 3 in human immune cells Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Differential expression of interferon-lambda receptor 1 splice variants determines the magnitude of the antiviral response induced by interferon-lambda 3 in human immune cells
Creator	Id, David Id, Michael Elahi, Shokrollah Golec, Dominic Namdar, Afshin Shah, Juhi Houghton Id, Michael Id, Julia Minty Id, Gillian Santer Id, Deanna Tyrrell Id, D
source	PMC
abstract	Type III interferons (IFN-lambdas(λ)) are important cytokines that inhibit viruses and modulate immune responses by acting through a unique IFN-λR1/IL-10RB heterodimeric receptor. Until now, the primary antiviral function of IFN-λs has been proposed to be at anatomical barrier sites. Here, we examine the regulation of IFN-λR1 expression and measure the downstream effects of IFN-λ3 stimulation in primary human blood immune cells, compared with lung or liver epithelial cells. IFN-λ3 directly bound and upregulated IFN-stimulated gene (ISG) expression in freshly purified human B cells and CD8(+) T cells, but not monocytes, neutrophils, natural killer cells, and CD4(+) T cells. Despite similar IFNLR1 transcript levels in B cells and lung epithelial cells, lung epithelial cells bound more IFN-λ3, which resulted in a 50-fold greater ISG induction when compared to B cells. The reduced response of B cells could be explained by higher expression of the soluble variant of IFN-λR1 (sIFN-λR1), which significantly reduced ISG induction when added with IFN-λ3 to peripheral blood mononuclear cells or liver epithelial cells. T-cell receptor stimulation potently, and specifically, upregulated membrane-bound IFNLR1 expression in CD4(+) T cells, leading to greater antiviral gene induction, and inhibition of human immunodeficiency virus type 1 infection. Collectively, our data demonstrate IFN-λ3 directly interacts with the human adaptive immune system, unlike what has been previously shown in published mouse models, and that type III IFNs could be potentially utilized to suppress both mucosal and blood-borne viral infections.
has issue date	2020-04-30(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1008515
bibo:pmid	32353085
has license	cc-by
sha1sum (hex)	f07169e2793ad34fd40d4e52675c0f584dcf2f9a
schema:url	https://doi.org/10.1371/journal.ppat.1008515
resource representing a document's title	Differential expression of interferon-lambda receptor 1 splice variants determines the magnitude of the antiviral response induced by interferon-lambda 3 in human immune cells
has PubMed Central identifier	PMC7217487
has PubMed identifier	32353085
schema:publication	PLoS Pathog
resource representing a document's body	covid:f07169e2793ad34fd40d4e52675c0f584dcf2f9a#body_text
is schema:about of	named entity 'peripheral blood mononuclear cells' named entity 'Despite' named entity 'liver' named entity 'compared' named entity 'human' named entity 'epithelial cells' named entity 'bound' named entity 'Here' named entity 'transcript' named entity 'purified' named entity 'induction' named entity 'cytokines' named entity 'blood-borne' named entity 'infection' named entity 'antiviral' named entity 'induced' named entity 'viruses' named entity 'monocytes' named entity 'gene' named entity 'epithelial cells' named entity 'antiviral' named entity 'adaptive immune' named entity 'lung' named entity 'membrane-bound' named entity 'human blood' named entity 'infection' named entity 'CD4 +' named entity 'IFNLR1' named entity 'receptor' named entity 'IFNLR1' named entity 'receptor' named entity 'interferon' named entity 'gene' named entity 'viruses' named entity 'clone' named entity 'TCR' named entity 'neutrophils' named entity 'Rockefeller University' named entity 'CD4 +' named entity 'cell types' named entity 'hepatocytes' named entity 'monocytes' named entity 'epithelial cells' named entity 'inflammatory conditions' named entity 'IFIT1' named entity 'Interferon' named entity 'IL10RB' named entity 'TRIzol' named entity 'IFNLR1' named entity 'cell surface' named entity 'NK cells' named entity 'IFNLR1' named entity 'upregulate' named entity 'regulatory mechanisms' named entity 'mouse model' named entity 'immune cells' named entity 'primates' named entity 'positive control' named entity 'immune cells' named entity 'CD4' named entity 'neutrophils' named entity 'Huh7' named entity 'mammals' named entity 'epithelial cells' named entity 'ligand' named entity 'TCR' named entity 'influenza virus' named entity 'CD56' named entity 'antibodies' named entity 'IFNLR1' named entity 'Interferon'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2025 OpenLink Software