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The Type I interferon response impairs differentiation potential of pluripotent stem cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE122794 | GEO | 2018/11/22

REPOSITORIES: GEO

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Type I interferon response impairs differentiation potential of pluripotent stem cells.

Project description:Upon virus infection, pluripotent stem cells neither induce nor respond to canonical type I interferons (IFN-I). To better understand this biology, we characterized induced pluripotent stem cells (iPSCs) as well as their differentiated parental or rederived counterparts. We confirmed that only iPSCs failed to respond to viral RNA, IFN-I, or viral infection. This lack of response could be phenocopied in fibroblasts with the expression of a reprogramming factor which repressed the capacity to induce canonical antiviral pathways. To ascertain the consequences of restoring the antiviral response in the context of pluripotency, we engineered a system to engage these defenses in iPSCs. Inducible expression of a recombinant virus-activated transcription factor resulted in the successful reconstitution of antiviral defenses through the direct up-regulation of IFN-I-stimulated genes. Induction of the antiviral signature in iPSCs, even for a short duration, resulted in the dysregulation of genes associated with all three germ layers despite maintaining pluripotency markers. Trilineage differentiation of these same cells showed that engagement of the antiviral defenses compromised ectoderm and endoderm formation and dysregulated the development of mesodermal sublineages. In all, these data suggest that the temporal induction of the antiviral response primes iPSCs away from pluripotency and induces numerous aberrant gene products upon differentiation. Together these results suggest that the IFN-I system and pluripotency may be incompatible with each other and thus explain why stem cells do not utilize the canonical antiviral system.

| S-EPMC6347712 | biostudies-literature

The Type I interferon response impairs differentiation potential of pluripotent stem cells [seq]

Project description:Upon virus infection,pluripotent stem cells neither induce nor respond to canonical Type I interferons (IFN-I). To better understand this biology,we characterized induced pluripotent stem cells (iPSCs) as well as their differentiated parental or re-derived counterparts. We confirmed that only iPSCs failed to respond to viral RNA,Type I interferon (IFN-I),or viral infection. This lack of response could be phenocopied in fibroblasts with the expression of a reprogramming factor which repressed the capacity to induce canonical antiviral pathways. To ascertain the consequences of restoring the antiviral response in the context of pluripotency,we engineered a system to engage these defenses in iPSCs. Inducible expression of a recombinant virus-activated transcription factor resulted in the successful reconstitution of antiviral defenses through the direct upregulation of IFN-I stimulated genes. Induction of the antiviral signature in iPSCs,even for a short duration,resulted in the dysregulation of genes associated with all three germ layers despite maintaining pluripotency markers. Trilineage differentiation of these same cells showed that engagement of the antiviral defenses compromised ectoderm and endoderm formation and dysregulated the development of mesodermal sublineages. In all,these data suggest that the temporal induction of the antiviral response primes iPSCs away from pluripotency and induces numerous aberrant gene products upon differentiaton. Together these results suggest that the IFN-I system and pluripotency may be incompatible with each other and thus explain why stem cells do not utilize the canonical antiviral system.

2018-11-22 | GSE122791 | GEO

The Type I interferon response impairs differentiation potential of pluripotent stem cells [RT-qPCR]

2018-11-22 | GSE122793 | GEO

The Type I interferon response impairs differentiation potential of pluripotent stem cells

Project description:The Type I interferon response impairs differentiation potential of pluripotent stem cells

| PRJNA506369 | ENA

The Type I interferon response impairs differentiation potential of pluripotent stem cells [seq]

Project description:The Type I interferon response impairs differentiation potential of pluripotent stem cells [seq]

| PRJNA506373 | ENA

The Type I interferon response impairs differentiation potential of pluripotent stem cells [RT-qPCR]

Project description:The Type I interferon response impairs differentiation potential of pluripotent stem cells [RT-qPCR]

| PRJNA506372 | ENA

Donor cell type influences the epigenome and differentiation potential of human induced pluripotent stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2011-11-29 | GSE27224 | GEO

Time-regulated transcripts with the potential to modulate human pluripotent stem cell-derived cardiomyocyte differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-15 | GSE188749 | GEO

Donor cell type influences the epigenome and differentiation potential of human induced pluripotent stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE27134: DNA methylation data from human iPS cells, ES cells, cord blood, and keratinocytes GSE27186: Expression data of human somatic cell types and induced pluripotent stem cells GSE31742: DNA methylation data from human keratinocyte-derived iPS cells (N9) and ES cells Refer to individual Series

2011-11-29 | E-GEOD-27224 | biostudies-arrayexpress

Characterization of type I interferon pathway during hepatic differentiation of human pluripotent stem cells and hepatitis C virus infection.

Project description:Pluripotent stem cells are being actively studied as a cell source for regenerating damaged liver. For long-term survival of engrafting cells in the body, not only do the cells have to execute liver-specific function but also withstand the physical strains and invading pathogens. The cellular innate immune system orchestrated by the interferon (IFN) pathway provides the first line of defense against pathogens. The objective of this study is to assess the innate immune function as well as to systematically profile the IFN-induced genes during hepatic differentiation of pluripotent stem cells. To address this objective, we derived endodermal cells (day 5 post-differentiation), hepatoblast (day 15) and hepatocyte-like cells (day 21) from human embryonic stem cells (hESCs). Day 5, 15 and 21 cells were stimulated with IFN-? and subjected to IFN pathway analysis. Transcriptome analysis was carried out by RNA sequencing. The results showed that the IFN-? treatment activated STAT-JAK pathway in differentiating cells. Transcriptome analysis indicated stage specific expression of classical and non-classical IFN-stimulated genes (ISGs). Subsequent validation confirmed the expression of novel ISGs including RASGRP3, CLMP and TRANK1 by differentiated hepatic cells upon IFN treatment. Hepatitis C virus replication in hESC-derived hepatic cells induced the expression of ISGs--LAMP3, ETV7, RASGRP3, and TRANK1. The hESC-derived hepatic cells contain intact innate system and can recognize invading pathogens. Besides assessing the tissue-specific functions for cell therapy applications, it may also be important to test the innate immune function of engrafting cells to ensure adequate defense against infections and improve graft survival.

| S-EPMC4600668 | biostudies-literature

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