Activation of TLR3/interferon signaling pathway by bluetongue virus results in HIV inhibition in macrophages

Background: Osteosarcoma (OS) is one of the most common primary malignant bone tumors in teenagers. Emerging studies demonstrated TWEAK and Fn14 were involved in regulating cancer cell differentiation, proliferation, apoptosis, migration and invasion. Objective: The present study identified differently expressed mRNAs and lncRNAs after anti-TWEAK treatment in OS cells using GSE41828. Methods: We identified 922 up-regulated mRNAs, 863 downregulated mRNAs, 29 up-regulated lncRNAs, and 58 down-regulated lncRNAs after anti-TWEAK treatment in OS cells. By constructing PPI networks, we identified several key proteins involved in anti-TWEAK treatment in OS cells, including MYC, IL6, CD44, ITGAM, STAT1, CCL5, FN1, PTEN, SPP1, TOP2A, and NCAM1. By constructing lncRNAs coexpression networks, we identified several key lncRNAs, including LINC00623, LINC00944, PSMB8-AS1, LOC101929787. Result: Bioinformatics analysis revealed DEGs after anti-TWEAK treatment in OS were involved in regulating type I interferon signaling pathway, immune response related pathways, telomere organization, chromatin silencing at rDNA, and DNA replication. Bioinformatics analysis revealed differently expressed lncRNAs after antiTWEAK treatment in OS were related to telomere organization, protein heterotetramerization, DNA replication, response to hypoxia, TNF signaling pathway, PI3K-Akt signaling pathway, Focal adhesion, Apoptosis, NF-kappa B signaling pathway, MAPK signaling pathway, FoxO signaling pathway. Conclusion: : This study provided useful information for understanding the mechanisms of TWEAK underlying OS progression and identifying novel therapeutic markers for OS.

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Cardiotrophin like cytokine factor 1 (CLCF1) alleviates bone loss in osteoporosis mouse models by suppressing osteoclast differentiation through activating interferon signaling and repressing the nuclear factor-κB signaling pathway

Bone ◽

10.1016/j.bone.2021.116140 ◽

2021 ◽

pp. 116140

Author(s):

Shunichi Yokota ◽

Gen Matsumae ◽

Tomohiro Shimizu ◽

Tomoka Hasegawa ◽

Taku Ebata ◽

...

Keyword(s):

Bone Loss ◽

Signaling Pathway ◽

Mouse Models ◽

Osteoclast Differentiation ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Interferon Signaling

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Bluetongue virus non-structural protein 3 (NS3) and NS4 coordinatively antagonize type Ⅰ interferon signaling by targeting STAT1

Veterinary Microbiology ◽

10.1016/j.vetmic.2021.108986 ◽

2021 ◽

Vol 254 ◽

pp. 108986

Author(s):

Zhuoran Li ◽

Danfeng Lu ◽

Heng Yang ◽

Zhuoyue Li ◽

Pei Zhu ◽

...

Keyword(s):

Bluetongue Virus ◽

Interferon Signaling ◽

Structural Protein

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Herpes Simplex Virus Type 1 Suppresses the Interferon Signaling Pathway by Inhibiting Phosphorylation of STATs and Janus Kinases during an Early Infection Stage

Virology ◽

10.1006/viro.2001.0941 ◽

2001 ◽

Vol 286 (1) ◽

pp. 119-124 ◽

Cited By ~ 74

Author(s):

Shin-ichi Yokota ◽

Noriko Yokosawa ◽

Toru Kubota ◽

Tatsuo Suzutani ◽

Itsuro Yoshida ◽

...

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Signaling Pathway ◽

Virus Type ◽

Herpes Simplex Virus Type ◽

Interferon Signaling ◽

Janus Kinases ◽

Simplex Virus ◽

Infection Stage

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TO005OPERATIONAL TOLERANCE IN KIDNEY TRANSPLANT RECIPIENTS: TOMOGRAM TRANSCRIPTOMIC STUDY

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa141.to005 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Ondrej Viklicky ◽

Jiri Klema ◽

Petra Mrazova ◽

Daniel Abramowicz ◽

Marc Abramowicz ◽

...

Keyword(s):

Signaling Pathway ◽

Kidney Transplant ◽

Type I Interferon ◽

Gene Annotation ◽

Interferon Γ ◽

Type I ◽

Transplant Recipients ◽

Interferon Signaling ◽

Kidney Transplant Recipients ◽

Operational Tolerance

Abstract Background and Aims TOMOGRAM, multicenter study founded by DESCARTES ERA/EDTA WG, aims to identify transcriptomic and genomic signatures of operational tolerance (OT) in recently identified cohort of OT kidney transplant recipients. Method RNA sequencing of peripheral blood was evaluated in 15 OT patients recently identified by TOMOGRAM consortium in 8 European countries, 23 stable patients (≥ 15 years on immunosuppression, STA), 14 CABMR patients (≥ 1 year, CR), 14 non-transplant CNI-treated patients and 14 healthy controls (HC). Differential expression was performed using DESEq2 and gene annotation analysis using Enrichr. Besides immunosuppression unadjusted model, robust negative-binomial regression model was created to adjust for immunosuppression intake. The models was trained on homogeneous group of STA patients. Results Using model unadjusted for immunosuppression, no differences in transcriptomic profiles between OT, STA and HC groups were identified. Nine transcripts were upregulated and 2 downregulated in OT compared CR group. The number of deregulated transcripts substantially increased when the model was adjusted for immunosuppression. Gene annotation analysis of top ranked deregulated 1109 transcripts (FC>2, adjusted p value <0.0001) showed deregulation of biological processes related to interferon-γ-mediated signaling pathway (p=1.4*10-5), response to cytokine (p=1.5*10-5), type I interferon signaling pathway (p=0.00036), regulation of I-kappaB kinase/NF-kappaB signaling (p=0.0021), cytokine-mediated signaling pathway (p=0.019) and neutrophil mediated immunity (p=0.033). While interferon-γ-mediated and type I interferon signaling were related to transcripts increased in CR, neutrophils associated transcripts were increased in OT. Analysis of cell types transcripts showed enrichment of CD19 B cells (p=1.6*10-9) in CR, while CD56NK cells (p=2.5*10-11) and CD8 T cells (p=1.6*10-11) transcripts predominated in OT. To reveal probability of operational tolerance inside STA group, 13 transcripts able to discriminate OT and CR cohorts with high AUC (>0.89) were used in PCA analysis (ADGRG3, ATG2A, GDPD5, IL16, MX2, SLA2, PRKD2, SLIRP, GNLY, SRCAP, ARGHAP9, IGHM, CD5). The high probability of OT signature was found in a single STA patient. Conclusion Contrary to previous reports which pointed out towards naïve B cell signatures, unique OT patients exhibit other specific immunosuppression-independent transcriptomic profiles.

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