Usp18 driven enforced viral replication in dendritic cells contributes to break of immunological tolerance in autoimmune diabetes.
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Potential viral pathogenic mechanism in human type 1 diabetesCEACAM1 induces B-cell survival and is essential for protective antiviral antibody productionDeficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infectionCD169+ macrophages are sufficient for priming of CTLs with specificities left out by cross-priming dendritic cells.USP18 Sensitivity of Peptide Transporters PEPT1 and PEPT2.USP18 lack in microglia causes destructive interferonopathy of the mouse brain.Suppression of USP18 Potentiates the Anti-HBV Activity of Interferon Alpha in HepG2.2.15 Cells via JAK/STAT Signaling.Virus-specific antibodies allow viral replication in the marginal zone, thereby promoting CD8(+) T-cell priming and viral controlImmunoactivation induced by chronic viral infection inhibits viral replication and drives immunosuppression through sustained IFN-I responses.CD169+ macrophages regulate PD-L1 expression via type I interferon and thereby prevent severe immunopathology after LCMV infection.Presentation of Autoantigen in Peripheral Lymph Nodes Is Sufficient for Priming Autoreactive CD8+ T Cells.Spatiotemporally restricted arenavirus replication induces immune surveillance and type I interferon-dependent tumour regression.Lessons from the mouse: potential contribution of bystander lymphocyte activation by viruses to human type 1 diabetes.STAT2 is an essential adaptor in USP18-mediated suppression of type I interferon signaling.Multiple functions of USP18.Gene expression profile after knockdown of USP18 in Hepg2.2.15 cells.Toso regulates differentiation and activation of inflammatory dendritic cells during persistence-prone virus infection.Enforced viral replication, a mechanism for immune activation.Identification of key genes and pathways in regulating immune‑induced diseases of dendritic cells by bioinformatic analysis.CEACAM1 promotes CD8+ T cell responses and improves control of a chronic viral infection.USP18 (UBP43) Abrogates p21-Mediated Inhibition of HIV-1
P2860
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P2860
Usp18 driven enforced viral replication in dendritic cells contributes to break of immunological tolerance in autoimmune diabetes.
description
2013 nî lūn-bûn
@nan
2013 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@ast
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@en
type
label
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@ast
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@en
prefLabel
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@ast
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@en
P2093
P2860
P1433
P1476
Usp18 driven enforced viral re ...... erance in autoimmune diabetes.
@en
P2093
Dong-Er Zhang
George Iliakis
Haifeng C Xu
Karl S Lang
Max Löhning
Mike Recher
Nadine Honke
Namir Shaabani
Philipp A Lang
P2860
P304
P356
10.1371/JOURNAL.PPAT.1003650
P577
2013-10-24T00:00:00Z