Log in

Relevant bibliographies by topics / Type I interferon pathway / Journal articles

To see the other types of publications on this topic, follow the link: Type I interferon pathway.

Journal articles on the topic 'Type I interferon pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Type I interferon pathway.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Aaronson, D. S., and C. M. Horvath. "The Type I Interferon Pathway." Science Signaling 2003, no. 197 (2003): cm12. http://dx.doi.org/10.1126/stke.2003.197.cm12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Crow, Mary K., Mikhail Olferiev, and Kyriakos A. Kirou. "Type I Interferons in Autoimmune Disease." Annual Review of Pathology: Mechanisms of Disease 14, no. 1 (2019): 369–93. http://dx.doi.org/10.1146/annurev-pathol-020117-043952.

Full text

Abstract:

Type I interferons, which make up the first cytokine family to be described and are the essential mediators of antivirus host defense, have emerged as central elements in the immunopathology of systemic autoimmune diseases, with systemic lupus erythematosus as the prototype. Lessons from investigation of interferon regulation following virus infection can be applied to lupus, with the conclusion that sustained production of type I interferon shifts nearly all components of the immune system toward pathologic functions that result in tissue damage and disease. We review recent data, mainly from

APA, Harvard, Vancouver, ISO, and other styles

3

Biskup, Edyta, Brian Daniel Larsen, Leonor Rib, et al. "Photochemotherapy Induces Interferon Type III Expression via STING Pathway." Cells 9, no. 11 (2020): 2452. http://dx.doi.org/10.3390/cells9112452.

Full text

Abstract:

DNA-damaging cancer therapies induce interferon expression and stimulate the immune system, promoting therapy responses. The immune-activating STING (Stimulator of Interferon Genes) pathway is induced when DNA or double-stranded RNA (dsRNA) is detected in the cell cytoplasm, which can be caused by viral infection or by DNA damage following chemo- or radiotherapy. Here, we investigated the responses of cutaneous T-cell lymphoma (CTCL) cells to the clinically applied DNA crosslinking photochemotherapy (combination of 8–methoxypsoralen and UVA light; 8–MOP + UVA). We showed that this treatment ev

APA, Harvard, Vancouver, ISO, and other styles

4

Watson, Samir, Lisanne Knol, Jeroen Witteveldt, and Sara Macias. "Crosstalk Between Mammalian Antiviral Pathways." Non-Coding RNA 5, no. 1 (2019): 29. http://dx.doi.org/10.3390/ncrna5010029.

Full text

Abstract:

As part of their innate immune response against viral infections, mammals activate the expression of type I interferons to prevent viral replication and dissemination. An antiviral RNAi-based response can be also activated in mammals, suggesting that several mechanisms can co-occur in the same cell and that these pathways must interact to enable the best antiviral response. Here, we will review how the classical type I interferon response and the recently described antiviral RNAi pathways interact in mammalian cells. Specifically, we will uncover how the small RNA biogenesis pathway, composed

APA, Harvard, Vancouver, ISO, and other styles

5

Volpi, Stefano, Jessica Tsui, Marcello Mariani, et al. "Type I interferon pathway activation in COPA syndrome." Clinical Immunology 187 (February 2018): 33–36. http://dx.doi.org/10.1016/j.clim.2017.10.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Iversen, Marie B., Nina Ank, Jesper Melchjorsen та Søren R. Paludan. "Expression of Type III Interferon (IFN) in the Vaginal Mucosa Is Mediated Primarily by Dendritic Cells and Displays Stronger Dependence on NF-κB than Type I IFNs". Journal of Virology 84, № 9 (2010): 4579–86. http://dx.doi.org/10.1128/jvi.02591-09.

Full text

Abstract:

ABSTRACT Interferons (IFNs) are induced as an initial response to viral infection after recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs). Here, we report that different PAMPs induce type I and III IFN expression at different ratios after mucosal administration in the vaginas of mice and that Toll-like receptor 9 (TLR9) stimulation evokes a particularly strong IFN-λ response, which is essential for optimal antiviral protection. Depletion of CD11c+ cells in vivo revealed that dendritic cells (DCs) in the vaginal epithelium are a key source of

APA, Harvard, Vancouver, ISO, and other styles

7

Feng, Jun, Paul D. De Jesus, Victoria Su, et al. "RIOK3 Is an Adaptor Protein Required for IRF3-Mediated Antiviral Type I Interferon Production." Journal of Virology 88, no. 14 (2014): 7987–97. http://dx.doi.org/10.1128/jvi.00643-14.

Full text

Abstract:

ABSTRACTDetection of cytosolic nucleic acids by pattern recognition receptors leads to the induction of type I interferons (IFNs) and elicits the innate immune response. We report here the identification of RIOK3 as a novel adaptor protein that is essential for the cytosolic nucleic acid-induced type I IFN production and for the antiviral response to gammaherpesvirus through two independent kinome-wide RNA interference screens. RIOK3 knockdown blocks both cytosolic double-stranded B-form DNA and double-stranded RNA-induced IRF3 activation and IFN-β production. In contrast, the overexpression o

APA, Harvard, Vancouver, ISO, and other styles

8

Suspitsin, E. N., R. K. Raupov, E. M. Kuchinskaya, and M. M. Kostik. "Analysis of interferon type I signature for differential diagnosis of diseases of the immune system ( review of literature)." Russian Clinical Laboratory Diagnostics 66, no. 5 (2021): 279–84. http://dx.doi.org/10.51620/0869-2084-2021-66-5-279-284.

Full text

Abstract:

Type 1 interferons (IFN1) are both key molecules of antiviral defense and potent inflammatory mediators. In 2003, increased expression of a variety of interferon 1-regulated genes was observed in a blood cells of patients with systemic lupus erythematosus (SLE). This phenomenon was called the type 1 interferon signature (IFN1-signature). Since then, expression patterns indicating the presence of an IFN1-signature were consistently detected in a range of monogenic and complex autoimmune and autoinflammatory conditions. A quantitative indicator reflecting the degree of hyperactivation of the IFN

APA, Harvard, Vancouver, ISO, and other styles

9

Harris, Bethany D., Srilalitha Kuruganti, Ashlesha Deshpande, Paul A. Goepfert, W. Winn Chatham, and Mark R. Walter. "Characterization of Type-I IFN subtype autoantibodies and activity in SLE serum and urine." Lupus 29, no. 9 (2020): 1095–105. http://dx.doi.org/10.1177/0961203320935976.

Full text

Abstract:

Background/objective Type-I interferons contribute to pathogenesis in systemic lupus erythematosus, including nephritis. Interferons consist of a family of 16 proteins yet are often characterized in patients without knowledge of the specific interferon subtypes involved. Different interferons may function in the kidneys, and other organs, relative to what is often measured in patient blood. Moreover, antibodies to interferons may potentially modulate systemic or organ-specific interferon activity. The aim of this study was to characterize global interferon activity levels and identify autoanti

APA, Harvard, Vancouver, ISO, and other styles

10

Pinal-Fernandez, Iago, Maria Casal-Dominguez, Assia Derfoul, et al. "Identification of distinctive interferon gene signatures in different types of myositis." Neurology 93, no. 12 (2019): e1193-e1204. http://dx.doi.org/10.1212/wnl.0000000000008128.

Full text

Abstract:

ObjectiveActivation of the type 1 interferon (IFN1) pathway is a prominent feature of dermatomyositis (DM) muscle and may play a role in the pathogenesis of this disease. However, the relevance of the IFN1 pathway in patients with other types of myositis such as the antisynthetase syndrome (AS), immune-mediated necrotizing myopathy (IMNM), and inclusion body myositis (IBM) is largely unknown. Moreover, the activation of the type 2 interferon (IFN2) pathway has not been comprehensively explored in myositis. In this cross-sectional study, our objective was to determine whether IFN1 and IFN2 path

APA, Harvard, Vancouver, ISO, and other styles

11

Mattson, Lina, Antonio Lentini, Danuta R. Gawel, et al. "Potential Involvement of Type I Interferon Signaling in Immunotherapy in Seasonal Allergic Rhinitis." Journal of Immunology Research 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/5153184.

Full text

Abstract:

Specific immunotherapy (SIT) reverses the symptoms of seasonal allergic rhinitis (SAR) in most patients. Recent studies report type I interferons shifting the balance between type I T helper cell (Th1) and type II T helper cells (Th2) towards Th2 dominance by inhibiting the differentiation of naive T cells into Th1 cells. As SIT is thought to cause a shift towards Th1 dominance, we hypothesized that SIT would alter interferon type I signaling. To test this, allergen and diluent challenged CD4+ T cells from healthy controls and patients from different time points were analyzed. The initial expe

APA, Harvard, Vancouver, ISO, and other styles

12

Peng, Tao, Swathi Kotla, Roger E. Bumgarner, and Kurt E. Gustin. "Human Rhinovirus Attenuates the Type I Interferon Response by Disrupting Activation of Interferon Regulatory Factor 3." Journal of Virology 80, no. 10 (2006): 5021–31. http://dx.doi.org/10.1128/jvi.80.10.5021-5031.2006.

Full text

Abstract:

ABSTRACT The type I interferon (IFN) response requires the coordinated activation of the latent transcription factors NF-κB, interferon regulatory factor 3 (IRF-3), and ATF-2, which in turn activate transcription from the IFN-β promoter. Synthesis and subsequent secretion of IFN-β activate the Jak/STAT signaling pathway, resulting in the transcriptional induction of the full spectrum of antiviral gene products. We utilized high-density microarrays to examine the transcriptional response to rhinovirus type 14 (RV14) infection in HeLa cells, with particular emphasis on the type I interferon resp

APA, Harvard, Vancouver, ISO, and other styles

13

Freitas, Maria Cecilia S., Yoichiro Uchida, Charles Lassman, Gabriel M. Danovitch, Ronald W. Busuttil, and Jerzy W. Kupiec-Weglinski. "Type I Interferon Pathway Mediates Renal Ischemia/Reperfusion Injury." Transplantation 92, no. 2 (2011): 131–38. http://dx.doi.org/10.1097/tp.0b013e318220586e.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Baechler, Emily C., Hatice Bilgic, and Ann M. Reed. "Type I interferon pathway in adult and juvenile dermatomyositis." Arthritis Research & Therapy 13, no. 6 (2011): 249. http://dx.doi.org/10.1186/ar3531.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Ware, Carl F., and Chris Benedict. "Innate B cells: oxymoron or validated concept?" F1000Research 1 (August 2, 2012): 8. http://dx.doi.org/10.12688/f1000research.1-8.v1.

Full text

Abstract:

B lymphocytes promote the initial innate interferon response to viral pathogens without the need for antigen receptor activation. B cell dependent IFN production requires the cytokine, lymphotoxin-β. The LTβ pathway is well known to regulate lymphoid organogenesis and homeostasis by differentiating stromal cells and macrophages. However, in response to viral pathogens these same B cell-regulated populations rapidly produce type 1 interferons. Thus, B cells act as innate effector cells via LTβ homeostatic pathways, which serve as innate host barriers to viral pathogens.

APA, Harvard, Vancouver, ISO, and other styles

16

Kim, Tae Hoon, Dong Sun Oh, Hi Eun Jung, Jun Chang та Heung Kyu Lee. "Plasmacytoid Dendritic Cells Contribute to the Production of IFN-β via TLR7-MyD88-Dependent Pathway and CTL Priming during Respiratory Syncytial Virus Infection". Viruses 11, № 8 (2019): 730. http://dx.doi.org/10.3390/v11080730.

Full text

Abstract:

Respiratory syncytial virus (RSV) is the leading cause of respiratory viral infection in infants and children, yet little is known about the antiviral response of plasmacytoid dendritic cells (pDCs) to RSV infection. We tracked the cellular source of interferon-β using interferon-β/yellow fluorescent protein (YFP) reporter mice and identified the signaling pathway activated by RSV that induces type I interferon production in pDCs and DCs. Results from in vitro analyses of RSV-stimulated bone marrow cells revealed that RSV induces interferon-β production in both pDCs and DCs. Kinetic analyses o

APA, Harvard, Vancouver, ISO, and other styles

17

Chee, Ana Virginia, and Bernard Roizman. "Herpes Simplex Virus 1 Gene Products Occlude the Interferon Signaling Pathway at Multiple Sites." Journal of Virology 78, no. 8 (2004): 4185–96. http://dx.doi.org/10.1128/jvi.78.8.4185-4196.2004.

Full text

Abstract:

ABSTRACT Earlier studies have shown that herpes simplex virus 1 (HSV-1) blocks the interferon response pathways, at least at two sites, by circumventing the effects of activation of protein kinase R by double-stranded RNA and interferon and through the degradation of promyelocytic leukemia protein (PML) since interferon has no antiviral effects in PML−/− cells. Here we report on two effects of viral genes on other sites of the interferon signaling pathway. (i) In infected cells, Jak1 kinase associated with interferon receptors and Stat2 associated with the interferon signaling pathway rapidly

APA, Harvard, Vancouver, ISO, and other styles

18

Darrah, Eric J., Kyle P. Stoltz, Mitchell Ledwith, and Vera L. Tarakanova. "ATM supports gammaherpesvirus replication by attenuating type I interferon pathway." Virology 510 (October 2017): 137–46. http://dx.doi.org/10.1016/j.virol.2017.07.014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Blank, Thomas, and Marco Prinz. "Type I interferon pathway in CNS homeostasis and neurological disorders." Glia 65, no. 9 (2017): 1397–406. http://dx.doi.org/10.1002/glia.23154.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Krug, Anne, Gary D. Luker, Winfried Barchet, David A. Leib, Shizuo Akira, and Marco Colonna. "Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9." Blood 103, no. 4 (2004): 1433–37. http://dx.doi.org/10.1182/blood-2003-08-2674.

Full text

Abstract:

Abstract Natural interferon-producing cells (IPCs) specialize in the production of high levels of type 1 interferons (IFNs) in response to encapsulated DNA and RNA viruses. Here we demonstrate that the secretion of type 1 IFN in response to herpes simplex virus type 1 (HSV-1) in vitro is mediated by the toll-like receptor 9 (TLR9)/MyD88 pathway. Moreover, IPCs produce interleukin-12 (IL-12) in response to HSV-1 in vitro, which is also dependent on TLR9/ MyD88 signaling. Remarkably, though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 or TLR9 are cap

APA, Harvard, Vancouver, ISO, and other styles

21

Zhao, Yunjuan, Yunliang Xie та Wangen Li. "Liraglutide Exerts Potential Anti-inflammatory Effect in Type 1 Diabetes by Inhibiting IFN-γ Production via Suppressing JAK-STAT Pathway". Endocrine, Metabolic & Immune Disorders - Drug Targets 19, № 5 (2019): 656–64. http://dx.doi.org/10.2174/1871530319666190301115654.

Full text

Abstract:

Background: Type 1 diabetes is a T cell-mediated autoimmune disease. Interferon γ plays a critical role in the pathogenesis of type 1 diabetes. Signal transducer and activator of transcription transduces type I interferon cytokines in T cells, leading to Th1 cell differentiation and production of interferon γ. Recent studies suggest that liraglutide reduces the plasma concentration of C-reative protein in patients with type 1 diabetes and protects β cell function in the non-obese diabetic mouse. Objective: The study aimed to explore the effect of glucagon-like peptide-1 analogue on interferon

APA, Harvard, Vancouver, ISO, and other styles

22

Lang, Xueting, Tiantian Tang, Tengchuan Jin, Chen Ding, Rongbin Zhou, and Wei Jiang. "TRIM65-catalized ubiquitination is essential for MDA5-mediated antiviral innate immunity." Journal of Experimental Medicine 214, no. 2 (2016): 459–73. http://dx.doi.org/10.1084/jem.20160592.

Full text

Abstract:

MDA5 plays a critical role in antiviral innate immunity by functioning as a cytoplasmic double-stranded RNA sensor that can activate type I interferon signaling pathways, but the mechanism for the activation of MDA5 is poorly understood. Here, we show that TRIM65 specifically interacts with MDA5 and promotes K63-linked ubiquitination of MDA5 at lysine 743, which is critical for MDA5 oligomerization and activation. Trim65 deficiency abolishes MDA5 agonist or encephalomyocarditis virus (EMCV)–induced interferon regulatory factor 3 (IRF3) activation and type I interferon production but has no eff

APA, Harvard, Vancouver, ISO, and other styles

23

Rostami-Nejad, Mohammad, Mostafa Rezaei-Tavirani, Mohammad-Mehdi Zadeh-Esmaeel, et al. "Assessment of Cytokine-Mediated Signaling Pathway Dysregulation in Arm Skin After CO2 Laser Therapy." Journal of Lasers in Medical Sciences 10, no. 4 (2019): 257–63. http://dx.doi.org/10.15171/jlms.2019.42.

Full text

Abstract:

Introduction: Laser therapy is known as an efficient approach in dermatology surgery. CO2 laser therapy is a gold standard treatment in skin surgery. This study aimed to evaluate the interferons change after CO2 laser surgery Methods: Significant differentially-expressed genes (DEGs) of arm skin after 7 days of treatment by the CO2 laser relative to the controls are downloaded from Gene Expression Omnibus (GEO) and are included in the protein-protein interaction network via a STRING database (an application of Cytoscape software). The central DEGs were identified and enriched via gene ontology

APA, Harvard, Vancouver, ISO, and other styles

24

Fullam, Anthony, Lili Gu, Yvette Höhn та Martina Schröder. "DDX3 directly facilitates IKKα activation and regulates downstream signalling pathways". Biochemical Journal 475, № 22 (2018): 3595–607. http://dx.doi.org/10.1042/bcj20180163.

Full text

Abstract:

DDX3 is a DEAD-box RNA helicase that we and others have previously implicated in antiviral immune signalling pathways leading to type I interferon (IFN) induction. We previously demonstrated that it directly interacts with the kinase IKKε (IκB kinase ε), enhances it activation, and then facilitates phosphorylation of the transcription factor IRF3 by IKKε. However, the TLR7/9 (Toll-like receptor 7/9)-mediated pathway, one of the most physiologically relevant IFN induction pathways, proceeds independently of IKKε or the related kinase TBK1 (TANK-binding kinase 1). This pathway induces type I IFN

APA, Harvard, Vancouver, ISO, and other styles

25

Li, Wei, Barry P. Katz, and Stanley M. Spinola. "Haemophilus ducreyi Lipooligosaccharides Induce Expression of the Immunosuppressive Enzyme Indoleamine 2,3-Dioxygenase via Type I Interferons and Tumor Necrosis Factor Alpha in Human Dendritic Cells." Infection and Immunity 79, no. 8 (2011): 3338–47. http://dx.doi.org/10.1128/iai.05021-11.

Full text

Abstract:

ABSTRACTHaemophilus ducreyicauses chancroid, a genital ulcer disease. In human inoculation experiments, most volunteers fail to clear the bacteria despite the infiltration of innate and adaptive immune cells to the infected sites. The immunosuppressive protein indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme in thel-tryptophan-kynurenine metabolic pathway. Tryptophan depletion and tryptophan metabolites contribute to pathogen persistence by inhibiting T cell proliferation, inducing T cell apoptosis, and promoting the expansion of FOXP3+regulatory T (Treg) cells. We previously found

APA, Harvard, Vancouver, ISO, and other styles

26

Lange, Philip T., Eric J. Darrah, Emily P. Vonderhaar, et al. "Type I Interferon Counteracts Antiviral Effects of Statins in the Context of Gammaherpesvirus Infection." Journal of Virology 90, no. 7 (2016): 3342–54. http://dx.doi.org/10.1128/jvi.02277-15.

Full text

Abstract:

ABSTRACTThe cholesterol synthesis pathway is a ubiquitous cellular biosynthetic pathway that is attenuated therapeutically by statins. Importantly, type I interferon (IFN), a major antiviral mediator, also depresses the cholesterol synthesis pathway. Here we demonstrate that attenuation of cholesterol synthesis decreases gammaherpesvirus replication in primary macrophagesin vitroand reactivation from peritoneal exudate cellsin vivo. Specifically, the reduced availability of the intermediates required for protein prenylation was responsible for decreased gammaherpesvirus replication in statin-t

APA, Harvard, Vancouver, ISO, and other styles

27

Morrison, Juliet M., and Vincent R. Racaniello. "Proteinase 2Apro Is Essential for Enterovirus Replication in Type I Interferon-Treated Cells." Journal of Virology 83, no. 9 (2009): 4412–22. http://dx.doi.org/10.1128/jvi.02177-08.

Full text

Abstract:

ABSTRACT The Picornaviridae family comprises a diverse group of small RNA viruses that cause a variety of human and animal diseases. Some of these viruses are known to induce cleavage of components of the innate immune system and to inhibit steps in the interferon pathway that lead to the production of type I interferon. There has been no study of the effect of picornaviral infection on the events that occur after interferons have been produced. To determine whether members of the Enterovirus genus can antagonize the antiviral activity of interferon-stimulated genes (ISGs), we pretreated cells

APA, Harvard, Vancouver, ISO, and other styles

28

Gong, Yuanjin, Chang Chang, Xi Liu, et al. "Stimulator of Interferon Genes Signaling Pathway and its Role in Anti-tumor Immune Therapy." Current Pharmaceutical Design 26, no. 26 (2020): 3085–95. http://dx.doi.org/10.2174/1381612826666200610183048.

Full text

Abstract:

Stimulator of interferon genes is an important innate immune signaling molecule in the body and is involved in the innate immune signal transduction pathway induced by pathogen-associated molecular patterns or damage-associated molecular patterns. Stimulator of interferon genes promotes the production of type I interferon and thus plays an important role in the innate immune response to infection. In addition, according to a recent study, the stimulator of interferon genes pathway also contributes to anti-inflammatory and anti-tumor reactions. In this paper, current researches on the Stimulato

APA, Harvard, Vancouver, ISO, and other styles

29

Xiang, Ying, Richard C. Condit, Sangeetha Vijaysri, Bertram Jacobs, Bryan R. G. Williams, and Robert H. Silverman. "Blockade of Interferon Induction and Action by the E3L Double-Stranded RNA Binding Proteins of Vaccinia Virus." Journal of Virology 76, no. 10 (2002): 5251–59. http://dx.doi.org/10.1128/jvi.76.10.5251-5259.2002.

Full text

Abstract:

ABSTRACT The vaccinia virus E3L gene encodes two double-stranded RNA binding proteins that promote viral growth and pathogenesis through suppression of innate immunity. To explore how E3L enables vaccinia virus to evade the interferon system, cells and mice deficient in the principal interferon-regulated antiviral enzymes, PKR and RNase L, were infected with wild-type vaccinia virus and strains of vaccinia virus from which E3L had been deleted (E3L-deleted strains). While wild-type virus was unaffected by RNase L and PKR, virus lacking E3L replicated only in the deficient cells. Nevertheless,

APA, Harvard, Vancouver, ISO, and other styles

30

Ghodke-Puranik, Yogita, and Timothy B. Niewold. "Genetics of the type I interferon pathway in systemic lupus erythematosus." International Journal of Clinical Rheumatology 8, no. 6 (2013): 657–69. http://dx.doi.org/10.2217/ijr.13.58.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Vakaloglou, Katerina M., та Clio P. Mavragani. "Activation of the type I interferon pathway in primary Sjögrenʼs syndrome". Current Opinion in Rheumatology 23, № 5 (2011): 459–64. http://dx.doi.org/10.1097/bor.0b013e328349fd30.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Mavragani, Clio P., and Mary K. Crow. "Activation of the type I interferon pathway in primary Sjogren’s syndrome." Journal of Autoimmunity 35, no. 3 (2010): 225–31. http://dx.doi.org/10.1016/j.jaut.2010.06.012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Gallucci, Stefania, Sowmya Meka, and Ana M. Gamero. "Abnormalities of the type I interferon signaling pathway in lupus autoimmunity." Cytokine 146 (October 2021): 155633. http://dx.doi.org/10.1016/j.cyto.2021.155633.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Barman, Tarani Kanta, Rachael Racine, Jesse L. Bonin, Danielle Califano, Sharon L. Salmon, and Dennis W. Metzger. "Sequential targeting of interferon pathways for increased host resistance to bacterial superinfection during influenza." PLOS Pathogens 17, no. 3 (2021): e1009405. http://dx.doi.org/10.1371/journal.ppat.1009405.

Full text

Abstract:

Bacterial co-infections represent a major clinical complication of influenza. Host-derived interferon (IFN) increases susceptibility to bacterial infections following influenza, but the relative roles of type-I versus type-II IFN remain poorly understood. We have used novel mouse models of co-infection in which colonizing pneumococci were inoculated into the upper respiratory tract; subsequent sublethal influenza virus infection caused the bacteria to enter the lungs and mediate lethal disease. Compared to wild-type mice or mice deficient in only one pathway, mice lacking both IFN pathways dem

APA, Harvard, Vancouver, ISO, and other styles

35

Li, Jianfeng, Yin Liu, and Xuming Zhang. "Murine Coronavirus Induces Type I Interferon in Oligodendrocytes through Recognition by RIG-I and MDA5." Journal of Virology 84, no. 13 (2010): 6472–82. http://dx.doi.org/10.1128/jvi.00016-10.

Full text

Abstract:

ABSTRACT The murine coronavirus mouse hepatitis virus (MHV) induced the expression of type I interferon (alpha/beta interferon [IFN-α/β]) in mouse oligodendrocytic N20.1 cells. This induction is completely dependent on virus replication, since infection with UV light-inactivated virus could no longer induce IFN-α/β. We show that MHV infection activated both transcription factors, the IFN regulatory factor 3 (IRF-3) and nuclear factor κB (NF-κB), as evidenced by phosphorylation and nuclear translocation of IRF-3 and an increased promoter binding activity for IRF-3 and NF-κB. Furthermore, the cy

APA, Harvard, Vancouver, ISO, and other styles

36

Song, Wuqi, Wenping Kao, Aixia Zhai, et al. "Borna disease virus nucleoprotein inhibits type I interferon induction through the interferon regulatory factor 7 pathway." Biochemical and Biophysical Research Communications 438, no. 4 (2013): 619–23. http://dx.doi.org/10.1016/j.bbrc.2013.08.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Harman, Andrew N., Najla Nasr, Alexandra Feetham, et al. "HIV Blocks Interferon Induction in Human Dendritic Cells and Macrophages by Dysregulation of TBK1." Journal of Virology 89, no. 13 (2015): 6575–84. http://dx.doi.org/10.1128/jvi.00889-15.

Full text

Abstract:

ABSTRACTDendritic cells (DCs) and macrophages are present in the tissues of the anogenital tract, where HIV-1 transmission occurs in almost all cases. These cells are both target cells for HIV-1 and represent the first opportunity for the virus to interfere with innate recognition. Previously we have shown that both cell types fail to produce type I interferons (IFNs) in response to HIV-1 but that, unlike T cells, the virus does not block IFN induction by targeting IFN regulatory factor 3 (IRF3) for cellular degradation. Thus, either HIV-1 inhibits IFN induction by an alternate mechanism or, l

APA, Harvard, Vancouver, ISO, and other styles

38

Ge, Rui, Yi Zhou, Rui Peng, et al. "Conservation of the STING-Mediated Cytosolic DNA Sensing Pathway in Zebrafish." Journal of Virology 89, no. 15 (2015): 7696–706. http://dx.doi.org/10.1128/jvi.01049-15.

Full text

Abstract:

ABSTRACTZebrafish (Danio rerio) is a unique potential model animal for dissecting innate immune signaling. Here we demonstrate that herpes simplex virus 1 (HSV-1) could infect zebrafish at its different developmental stages and trigger the expression of type I interferons (IFNs) as well as interferon-stimulated genes (ISGs) in zebrafish larvae. Silencing of zSTING, but not zMAVS, markedly attenuates the DNA virus-induced antiviral responses. Notably, a conserved serine residue (S373) is essential for the action of zSTING. Unexpectedly, zebrafish cyclic GMP-AMP synthase (cGAS) is dispensable fo

APA, Harvard, Vancouver, ISO, and other styles

39

Le-Thi-Phuong, Thao, Gaëtan Thirion, and Jean-Paul Coutelier. "Distinct gamma interferon-production pathways in mice infected with lactate dehydrogenase-elevating virus." Journal of General Virology 88, no. 11 (2007): 3063–66. http://dx.doi.org/10.1099/vir.0.83242-0.

Full text

Abstract:

Two distinct pathways of gamma interferon (IFN-γ) production have been found in mice infected with lactate dehydrogenase-elevating virus. Both pathways involve natural killer cells. The first is mostly interleukin-12-independent and is not controlled by type I interferons. The second, which is suppressed by type I interferons, leads to increased levels of IFN-γ production and requires the secretion of interleukin-12. This regulation of IFN-γ production by type I interferons may help to control indirect pathogenesis induced by this cytokine.

APA, Harvard, Vancouver, ISO, and other styles

40

Schabmeyer, Simone Tamara, Anna Maria Kneidl, Julia Katharina Schneider, et al. "Concentration-Dependent Type 1 Interferon-Induced Regulation of MX1 and FABP3 in Bovine Endometrial Explants." Animals 11, no. 2 (2021): 262. http://dx.doi.org/10.3390/ani11020262.

Full text

Abstract:

The inadequate maternal recognition of embryonic interferon τ (IFNτ) might explain subfertility in cattle. This study aimed at modeling the inducibility of type 1 interferon receptor subunits 1/2 (IFNAR1/2), mimicking competition between IFNτ and infection-associated interferon α (IFNα), and simulating type 1 interferon pathways in vitro. Endometrial explants (n = 728 from n = 26 healthy uteri) were collected at the abattoir, challenged with IFNτ and/or IFNα in different concentrations, and incubated for 24 h. Gene expression analysis confirmed the inducibility of IFNAR1/2 within this model, i

APA, Harvard, Vancouver, ISO, and other styles

41

Flammer, Jamie R., Jana Dobrovolna, Megan A. Kennedy, et al. "The Type I Interferon Signaling Pathway Is a Target for Glucocorticoid Inhibition." Molecular and Cellular Biology 30, no. 19 (2010): 4564–74. http://dx.doi.org/10.1128/mcb.00146-10.

Full text

Abstract:

ABSTRACT Type I interferon (IFN) is essential for host defenses against viruses; however, dysregulated IFN signaling is causally linked to autoimmunity, particularly systemic lupus erythematosus. Autoimmune disease treatments rely on glucocorticoids (GCs), which act via the GC receptor (GR) to repress proinflammatory cytokine gene transcription. Conversely, cytokine signaling through cognate Jak/STAT pathways is reportedly unaffected or even stimulated by GR. Unexpectedly, we found that GR dramatically inhibited IFN-stimulated gene (ISG) expression in macrophages. The target of inhibition, the

APA, Harvard, Vancouver, ISO, and other styles

42

Amouzegar, Afsaneh, Manoj Chelvanambi, Jessica N. Filderman, Walter J. Storkus, and Jason J. Luke. "STING Agonists as Cancer Therapeutics." Cancers 13, no. 11 (2021): 2695. http://dx.doi.org/10.3390/cancers13112695.

Full text

Abstract:

The interrogation of intrinsic and adaptive resistance to cancer immunotherapy has identified lack of antigen presentation and type I interferon signaling as biomarkers of non-T-cell-inflamed tumors and clinical progression. A myriad of pre-clinical studies have implicated the cGAS/stimulator of interferon genes (STING) pathway, a cytosolic DNA-sensing pathway that drives activation of type I interferons and other inflammatory cytokines, in the host immune response against tumors. The STING pathway is also increasingly understood to have other anti-tumor functions such as modulation of the vas

APA, Harvard, Vancouver, ISO, and other styles

43

Vitour, Damien, Virginie Doceul, Suzana Ruscanu, Emilie Chauveau, Isabelle Schwartz-Cornil, and Stéphan Zientara. "Induction and control of the type I interferon pathway by Bluetongue virus." Virus Research 182 (March 2014): 59–70. http://dx.doi.org/10.1016/j.virusres.2013.10.027.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Ekholm, L., S. Vosslamber, A. Tjärnlund, et al. "Autoantibody Specificities and Type I Interferon Pathway Activation in Idiopathic Inflammatory Myopathies." Scandinavian Journal of Immunology 84, no. 2 (2016): 100–109. http://dx.doi.org/10.1111/sji.12449.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Taylor, Juliet M., Zachery Moore, Myles R. Minter, and Peter J. Crack. "Type-I interferon pathway in neuroinflammation and neurodegeneration: focus on Alzheimer’s disease." Journal of Neural Transmission 125, no. 5 (2017): 797–807. http://dx.doi.org/10.1007/s00702-017-1745-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Flammer, Jamie R., Megan A. Kennedy, Yurii Chinenov, Lionel B. Ivashkiv, and Inez Rogatsky. "187 Glucocorticoid regulation of the type I interferon-JAK/STAT signaling pathway." Cytokine 43, no. 3 (2008): 283–84. http://dx.doi.org/10.1016/j.cyto.2008.07.249.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Roy, Ethan, Baiping Wang, Hui Zheng, and Wei Cao. "TYPE I INTERFERON-MEDIATED NEUROINFLAMMATORY PROGRAM AND SYNAPSE LOSS IN ALZHEIMER’S DISEASE." Innovation in Aging 3, Supplement_1 (2019): S92. http://dx.doi.org/10.1093/geroni/igz038.349.

Full text

Abstract:

Abstract The cytokine family type I interferon (IFN) is a major innate immune mediator extensively studied in the peripheral immune responses but largely under-investigated in AD. Previously, we established that innate immune cells readily produce IFN in response to amyloid fibrils containing nucleic acids as cofactor. Here, we investigated whether IFN pathway is associated with amyloidosis in AD brain and contributes to neuroinflammation. By systemically characterizing neuroinflammation in multiple murine AD models, we established a comprehensive core AD neuroinflammation profile that include

APA, Harvard, Vancouver, ISO, and other styles

48

Simoni, Michael K., Sydnie Swanson, Monica Mainigi, and Kellie Jurado. "22732 Impact of Type-I Interferon Manipulation During Embryo Implantation and Placentation." Journal of Clinical and Translational Science 5, s1 (2021): 94–95. http://dx.doi.org/10.1017/cts.2021.644.

Full text

Abstract:

ABSTRACT IMPACT: This research will promote understanding the role of the Type-I Interferon signaling pathway during embryo implantation, potentially leading to a new diagnostic or treatment target in early pregnancy failure. OBJECTIVES/GOALS: Studies suggest interferon signaling regulation is tightly balanced between physiologic and pathophysiologic growth in early pregnancy. We propose to determine the impact of interferon-mediated inflammation on embryo implantation and early pregnancy failure in normal conditions and chronic inflammatory diseases in a novel mixed-mouse model. METHODS/STUDY

APA, Harvard, Vancouver, ISO, and other styles

49

Eisemann, Jutta, Petra Mühl-Zürbes, Alexander Steinkasserer, and Mirko Kummer. "Infection of mature dendritic cells with herpes simplex virus type 1 interferes with the interferon signaling pathway." Immunobiology 212, no. 9-10 (2008): 877–86. http://dx.doi.org/10.1016/j.imbio.2007.09.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Zhou, Zhangle, Ole J. Hamming, Nina Ank, Søren R. Paludan, Anders L. Nielsen, and Rune Hartmann. "Type III Interferon (IFN) Induces a Type I IFN-Like Response in a Restricted Subset of Cells through Signaling Pathways Involving both the Jak-STAT Pathway and the Mitogen-Activated Protein Kinases." Journal of Virology 81, no. 14 (2007): 7749–58. http://dx.doi.org/10.1128/jvi.02438-06.

Full text

Abstract:

ABSTRACT Type III interferon (IFN) is a novel member of the interferon family. Type III IFN utilizes a receptor complex different from that of type I IFN, but both types of IFN induce STAT1, STAT2, and STAT3 activation. Here we describe a detailed comparison of signal transduction initiated by type I and type III IFN. Gene expression array analysis showed that IFN types I and III induced a similar subset of genes. In particular, no genes were induced uniquely by type III IFN. Next, we used chromatin immunoprecipitation (ChIP) analysis to investigate the promoter activation by types I and III I

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!