scholarly journals Bovine Interferon-Tau Activates Type I interferon-Associated Janus-signal Transducer in HPV16-positive Tumor Cell

2020 ◽  
Vol 11 (16) ◽  
pp. 4754-4761
Author(s):  
Geny Fierros-Zárate ◽  
Clarita Olvera ◽  
Gustavo Salazar-Guerrero ◽  
Ausencio Morales-Ortega ◽  
Fernando Reyna ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Type I Interferon ◽  
Type I ◽  
Signal Transducer ◽  
Interferon Tau ◽  
Positive Tumor Cell

scholarly journals Growth sensitivity of a recombinant simian virus 5 P/V mutant to type I interferon differs between tumor cell lines and normal primary cells

Virology ◽  
2005 ◽  
Vol 335 (1) ◽  
pp. 131-144 ◽  
Author(s):  
Elizabeth K. Wansley ◽  
Patrick J. Dillon ◽  
Maria D. Gainey ◽  
James Tam ◽  
Scott D. Cramer ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Type I Interferon ◽  
Simian Virus ◽  
Type I ◽  
Tumor Cell Lines ◽  
Primary Cells ◽  
Simian Virus 5

scholarly journals Association between anti-interferon-alpha autoantibodies and COVID-19 in systemic lupus erythematosus

2020 ◽  
Author(s):  
Sarthak Gupta ◽  
Shuichiro Nakabo ◽  
Jun Chu ◽  
Sarfaraz Hasni ◽  
Mariana J. Kaplan
Keyword(s):  
Systemic Lupus Erythematosus ◽  
General Population ◽  
Lupus Erythematosus ◽  
Preventive Measures ◽  
Type I Interferon ◽  
Type I ◽  
List Type ◽  
Signal Transducer ◽  
Systemic Lupus

AbstractObjectivesAnti-type I interferon (IFN) autoantibodies have been reported in patients with systemic lupus erythematosus (SLE). Recently, an association of these autoantibodies with severe COVID-19 was reported in the general population. We assessed whether having pre-existing anti-IFNα autoantibodies was associated with COVID-19 infection in SLE patients.MethodsPatients with SLE who developed COVID-19 between April 1st to October 1st, 2020 were studied. Biobanked pre-COVID-19 plasma from these SLE subjects and healthy controls were tested for anti-IFNα IgG autoantibodies by ELISA. The ability of plasma anti-IFNα autoantibodies to block signal transducer and activator of transcription 1 (STAT1) phosphorylation by recombinant human IFNα in vitro was assessed by flow cytometry.ResultsTen SLE subjects with COVID-19 were identified. A 40% of these subjects had stable autoantibodies against IFNα for up to three years preceding COVID-19 diagnosis. A 50% of the subjects with these autoantibodies neutralized IFNα induced STAT1 phosphorylation.None of the other SLE samples blocked IFNα signaling.ConclusionsWe noted an increased prevalence of pre-existing anti-IFNα autoantibodies in SLE patients with COVID-19 compared to the reported prevalence in lupus patients and the general population with severe COVID-19. Autoantibodies against IFNα in SLE patients may be pathogenic and patients with them maybe at-risk of developing COVID-19.Key MessagesWhat is already known about this subject?-Anti-type I interferon (IFN) autoantibodies have been reported in patients with systemic lupus erythematosus (SLE) and have recently been associated with severe COVID-19 in the general population.What does this study add?-SLE subjects with COVID-19 had an increased prevalence of pre-existing anti-IFNα autoantibodies compared to the reported prevalence in lupus patients and the general population with severe COVID-19.-Plasma from 50% of subjects with these autoantibodies were able to block in vitro activity of IFNα.-SLE patients with pre-existing anti-IFNα autoantibodies had more severe COVID-19 manifestations.How might this impact on clinical practice or future developments?-Anti-IFNα autoantibodies may be pathogenic and could prove to be a helpful prognostic marker to predict which SLE patient may develop COVID-19 and inform preventive measures and management of this subset of patients.

scholarly journals Novel chemical compound SINCRO with dual function in STING ‐type I interferon and tumor cell death pathways

2018 ◽  
Vol 109 (9) ◽  
pp. 2687-2696 ◽  
Author(s):  
Yoshitaka Kimura ◽  
Hideo Negishi ◽  
Atsushi Matsuda ◽  
Nobuyasu Endo ◽  
Sho Hangai ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Chemical Compound ◽  
Type I Interferon ◽  
Dual Function ◽  
Type I ◽  
Tumor Cell Death ◽  
Cell Death Pathways

scholarly journals The evolution of interferon-tau

Reproduction ◽  
2017 ◽  
Vol 154 (5) ◽  
pp. F1-F10 ◽  
Author(s):  
Alan D Ealy ◽  
Lydia K Wooldridge
Keyword(s):  
Biological Activity ◽  
Molecular Cloning ◽  
Type I Interferon ◽  
Cdna Libraries ◽  
Type I ◽  
Interferon Tau ◽  
Sheep And Goats ◽  
Type I Ifns

Thirty years ago, a novel type I interferon (IFN) was identified by molecular cloning of cDNA libraries constructed from RNA extracted from ovine and bovine pre-implantation embryos. This protein was eventually designated as IFN-tau (IFNT) to highlight its trophoblast-dependent expression. IFNT function is not immune related. Instead, it interacts with the maternal system to initiate the establishment and maintenance of pregnancy. This activity is indispensable for the continuation of pregnancy. Our review will describe how IFNT evolved from other type I IFNs to function in this new capacity. IFNT genes have only been identified in pecoran ruminants within the Artiodactyla order (e.g. cattle, sheep, goats, deer, antelope, giraffe). The ancestral IFNT gene emerged approximately 36 million years ago most likely from rearrangement and/or insertion events that combined an ancestral IFN-omega (IFNW) gene with a trophoblast-specifying promoter/enhancer. Since then, IFNT genes have duplicated, likely through conversion events, and mutations have allowed them to adapt to their new function in concert with the emergence of different species. Multiple IFNT polymorphisms have been identified in cattle, sheep and goats. These genes and gene alleles encode proteins that do not display identical antiviral, antiproliferative and antiluteolytic activities. The need for multiple IFNT genes, numerous alleles and distinct activities remains debatable, but the consensus is that this complexity in IFNT expression and biological activity must be needed to provide the best opportunity for pregnancy to be recognized by the maternal system so that gestation may continue.

scholarly journals Human Cytomegalovirus UL23 Attenuates Signal Transducer and Activator of Transcription 1 Phosphorylation and Type I Interferon Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Linyuan Feng ◽  
Wanwei Li ◽  
Xingyuan Wu ◽  
Xiaotian Li ◽  
Xiaoping Yang ◽  
...  
Keyword(s):  
Human Cytomegalovirus ◽  
Type I Interferon ◽  
Signal Transduction Pathway ◽  
Interferon Response ◽  
Type I ◽  
Signal Transducer ◽  
Tyrosine Kinase 2 ◽  
Disease Occurrence ◽  
Key Factor ◽  
Determining Factor

Human cytomegalovirus (HCMV), the human beta-herpesvirus, can cause severe syndromes among both immunocompromised adult patients and newborns. Type I interferon (IFN-I) exerts an important effect to resist infections caused by viruses such as HCMV, while IFN evasion may serve as a key determining factor for viral dissemination and disease occurrence within hosts. In this study, UL23, a tegument protein of HCMV, was confirmed to be a key factor for negatively regulating the type I IFN immune response. A detailed analysis indicated that the viral UL23 protein increases the IFN-I antiviral resistance during HCMV infections. Furthermore, UL23 was shown to significantly reduce the levels of IFN-stimulated genes (ISGs) and promoter activity of IFN-I-stimulated response element. Mechanically, UL23 was discovered to impair the signal transducer and activator of transcription 1 (STAT1) phosphorylation, although it was not found to affect phosphorylation and expression of STAT2, Janus activated kinase 1, or tyrosine kinase 2, which are associated with IFN-I signal transduction pathway. Additionally, a significantly reduced nuclear expression of STAT1 but not of IFN regulatory factor 9 or STAT2 was observed. Findings of this study indicate that HCMV UL23 is a viral antagonist that acts against the cellular innate immunity and reveal a possible novel effect of UL23 on IFN-I signaling.

scholarly journals Suppression of Type I Interferon Signaling by Flavivirus NS5

Viruses ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 712 ◽  
Author(s):  
Stephanie Thurmond ◽  
Boxiao Wang ◽  
Jikui Song ◽  
Rong Hai
Keyword(s):  
Host Defense ◽  
Type I Interferon ◽  
Mammalian Host ◽  
Type I ◽  
Signal Transducer ◽  
Type I Ifn ◽  
Interferon Signaling ◽  
Structural Protein ◽  
First Line

Type I interferon (IFN-I) is the first line of mammalian host defense against viral infection. To counteract this, the flaviviruses, like other viruses, have encoded a variety of antagonists, and use a multi-layered molecular defense strategy to establish their infections. Among the most potent antagonists is non-structural protein 5 (NS5), which has been shown for all disease-causing flaviviruses to target different steps and players of the type I IFN signaling pathway. Here, we summarize the type I IFN antagonist mechanisms used by flaviviruses with a focus on the role of NS5 in regulating one key regulator of type I IFN, signal transducer and activator of transcription 2 (STAT2).

scholarly journals The in vivo antitumor effects of type I-interferon against hepatocellular carcinoma: the suppression of tumor cell growth and angiogenesis

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Hirayuki Enomoto ◽  
Lihua Tao ◽  
Ryoji Eguchi ◽  
Ayuko Sato ◽  
Masao Honda ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Tumor Cell ◽  
Type I Interferon ◽  
Type I ◽  
Tumor Cell Growth ◽  
Antitumor Effects

scholarly journals Regulation of Tripartite Motif-Containing Proteins on Immune Response and Viral Evasion

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiu-Zhong Zhang ◽  
Fu-Huang Li ◽  
Xiao-Jia Wang
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Signaling Pathways ◽  
Type I Interferon ◽  
Janus Kinase ◽  
Host Cells ◽  
Type I ◽  
Signal Transducer ◽  
Ubiquitin E3 Ligase ◽  
Tripartite Motif

Tripartite motif-containing proteins (TRIMs), exhibiting ubiquitin E3 ligase activity, are involved in regulation of not only autophagy and apoptosis but also pyrotosis and antiviral immune responses of host cells. TRIMs play important roles in modulating signaling pathways of antiviral immune responses via type I interferon, NF-κB, Janus kinase/signal transducer and activator of transcription (JAK/STAT), and Nrf2. However, viruses are able to antagonize TRIM activity or evenly utilize TRIMs for viral replication. This communication presents the current understanding of TRIMs exploited by viruses to evade host immune response.

scholarly journals Blockade of Type I Interferon (IFN) Production by Retroviral Replicating Vectors and Reduced Tumor Cell Responses to IFN Likely Contribute To Tumor Selectivity

2014 ◽  
Vol 88 (17) ◽  
pp. 10066-10077 ◽  
Author(s):  
A. H. Lin ◽  
C. Burrascano ◽  
P. L. Pettersson ◽  
C. E. Ibanez ◽  
H. E. Gruber ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Type I Interferon ◽  
Type I ◽  
Cell Responses ◽  
Tumor Selectivity
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