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Journal articles on the topic 'Interferons (IFNs)'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 September 2023

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1

Bruening, Janina, Bettina Weigel, and Gisa Gerold. "The Role of Type III Interferons in Hepatitis C Virus Infection and Therapy." Journal of Immunology Research 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/7232361.

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The human interferon (IFN) response is a key innate immune mechanism to fight virus infection. IFNs are host-encoded secreted proteins, which induce IFN-stimulated genes (ISGs) with antiviral properties. Among the three classes of IFNs, type III IFNs, also called IFN lambdas (IFNLs), are an essential component of the innate immune response to hepatitis C virus (HCV). In particular, human polymorphisms in IFNL gene loci correlate with hepatitis C disease progression and with treatment response. To date, the underlying mechanisms remain mostly elusive; however it seems clear that viral infection

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2

Abdolvahab, Mohadeseh Haji, Behrad Darvishi, Mohammad Zarei, Keivan Majidzadeh-A, and Leila Farahmand. "Interferons: role in cancer therapy." Immunotherapy 12, no. 11 (2020): 833–55. http://dx.doi.org/10.2217/imt-2019-0217.

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Interferons (IFNs) are a group of signaling cytokines, secreted by host cells to induce protection against various disorders. IFNs can directly impact on tumor cells or indirectly induce the immune system to protect host cells. The expression levels of IFNs and its functions of are excellently modulated in a way to protect host cells from probable toxicities caused by extreme responses. The efficacy of anticancer therapies is correlated to IFNs signaling. Although IFN signaling is involved in induction of antitumor responses, chronic stimulation of the IFN signaling pathway can induce resistan

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3

Tilg, Herbert, and Arthur Kaser. "Interferons and Their Role in Inflammation." Current Pharmaceutical Design 5, no. 10 (1999): 771–85. http://dx.doi.org/10.2174/1381612805666230111210939.

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Cytokines are pleiotropic molecules showing a wide variety of biologic functions on various cells and tissues, and several different cytokines exert similar and overlapping functions on certain cells. Interferons (IFNs), among the first cytokines identified, play a crucial role in human disease. The IFN cytokine family consists of type I IFNs (IFN-a and IFN- ) and type II IFN (IFN-y). In the first decades of IFN research, type I IFNs were considered primarily as viral inhibitors, whereas type II IFN, also termed "immune IFN", was generally considered to be uniquely involved in immune reactions

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Manry, Jérémy, Guillaume Laval, Etienne Patin, et al. "Evolutionary genetic dissection of human interferons." Journal of Experimental Medicine 208, no. 13 (2011): 2747–59. http://dx.doi.org/10.1084/jem.20111680.

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Interferons (IFNs) are cytokines that play a key role in innate and adaptive immune responses. Despite the large number of immunological studies of these molecules, the relative contributions of the numerous IFNs to human survival remain largely unknown. Here, we evaluated the extent to which natural selection has targeted the human IFNs and their receptors, to provide insight into the mechanisms that govern host defense in the natural setting. We found that some IFN-α subtypes, such as IFN-α6, IFN-α8, IFN-α13, and IFN-α14, as well as the type II IFN-γ, have evolved under strong purifying sele

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Samuel, Charles E. "Antiviral Actions of Interferons." Clinical Microbiology Reviews 14, no. 4 (2001): 778–809. http://dx.doi.org/10.1128/cmr.14.4.778-809.2001.

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SUMMARY Tremendous progress has been made in understanding the molecular basis of the antiviral actions of interferons (IFNs), as well as strategies evolved by viruses to antagonize the actions of IFNs. Furthermore, advances made while elucidating the IFN system have contributed significantly to our understanding in multiple areas of virology and molecular cell biology, ranging from pathways of signal transduction to the biochemical mechanisms of transcriptional and translational control to the molecular basis of viral pathogenesis. IFNs are approved therapeutics and have moved from the basic

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6

Kimura, M., J. A. Majde, L. A. Toth, M. R. Opp, and J. M. Krueger. "Somnogenic effects of rabbit and recombinant human interferons in rabbits." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (1994): R53—R61. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r53.

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Interferons (IFNs) are antiviral cytokines that possess several central nervous system activities. IFN therapy is associated with sleepiness, and the IFNs expressed during viral infection may be involved in the excess sleep associated with these infections. Most viruses stimulate the production of both IFN-alpha and IFN-beta. Although large doses of human IFN-alpha 2 are somnogenic in rabbits, the effects of species-specific IFNs on sleep in the rabbit have not been documented. We compared the somnogenic and antiviral effects of IFNs derived from rabbits to the effects of recombinant human (rh

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7

Asselin-Paturel, Carine, and Giorgio Trinchieri. "Production of type I interferons." Journal of Experimental Medicine 202, no. 4 (2005): 461–65. http://dx.doi.org/10.1084/jem.20051395.

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Plasmacytoid dendritic cells (pDCs) are specialized producers of type I interferons (IFNs) that respond to most viruses. Because of their antiviral activity and regulatory functions in innate and adaptive immunity, type I IFNs are important not only for antiviral resistance but also in other types of infections and in immune pathology. Here we discuss recent data that begin to reveal the unique molecular mechanisms underlying the remarkably rapid and efficient type I IFN production by pDCs.

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8

Sinkovics, Joseph G. "Interferons: Antiangiogenesis Agents (A Reasonable Theory)." Canadian Journal of Infectious Diseases 3, suppl b (1992): 128–32. http://dx.doi.org/10.1155/1992/754560.

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Antiviral and immunomodulatory effects of interferons (IFNs) are well-known. This communication lists arguments for explicit antiangiogenetic effects exerted by interferons. There is strong likelihood that IFNs α, β and γ inhibit the int family of genes whose gene product proteins are the acidic and basic fibroblast growth factors. Some of these growth factors promote the growth of vascular endothelial cells. IFN-α inhibits basic, and IFN-γ inhibits acidic fibroblast growth factors. Inhibition of Kaposi sarcoma cell growth is not due to immunological reconstitution of the host. As IFN-α induce

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9

Mundra, Akaash, Aram Yegiazaryan, Haig Karsian, et al. "Pathogenicity of Type I Interferons in Mycobacterium tuberculosis." International Journal of Molecular Sciences 24, no. 4 (2023): 3919. http://dx.doi.org/10.3390/ijms24043919.

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Tuberculosis (TB) is a leading cause of mortality due to infectious disease and rates have increased during the emergence of COVID-19, but many of the factors determining disease severity and progression remain unclear. Type I Interferons (IFNs) have diverse effector functions that regulate innate and adaptive immunity during infection with microorganisms. There is well-documented literature on type I IFNs providing host defense against viruses; however, in this review, we explore the growing body of work that indicates high levels of type I IFNs can have detrimental effects to a host fighting

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10

Plata-Salaman, C. R. "Interferons and central regulation of feeding." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 6 (1992): R1222—R1227. http://dx.doi.org/10.1152/ajpregu.1992.263.6.r1222.

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Interferons (IFNs) are immunomodulators with neuromodulatory activities. To study the effects of IFNs on the central regulation of feeding, rats were subjected to various applications. The results show the following. 1) Intracerebroventricular microinfusion of rat IFN (15-225 IU/rat) decreased short-term (2-h) food intake in rats. Computerized analysis of behavioral patterns demonstrated a reduction of meal size and meal duration, whereas meal frequency slightly increased. Nighttime and total daily food intakes were not significantly affected. 2) Short-term food intake suppression by intracere

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11

Sherwani, Mohammad Asif, Israr Ahmad, Chander Raman, Craig Elmets, and Nabiha Yusuf. "Regulation of ultraviolet radiation-induced cutaneous DNA damage by type I interferons." Journal of Immunology 204, no. 1_Supplement (2020): 162.9. http://dx.doi.org/10.4049/jimmunol.204.supp.162.9.

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Abstract Type I interferons (IFNs) are cytokines, that are important regulators of immune responses and are downregulated in human cancers, including skin cancer. Solar ultraviolet (UV) radiation is a proven environmental carcinogen, and exposure to solar radiation contributes to the high prevalence of skin cancer. The carcinogenic effects of UV light can be attributed to the formation of cyclobutane pyrimidine dimers (CPD) and errors in repair and replication of DNA. It is believed that type I IFNs reduce cellular proliferation and allow DNA repair in various diseases. Interferon receptor 1 (

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12

Chin, Kai Ling, Fadhilah Zulkipli Anis, Maria E. Sarmiento, Mohd Nor Norazmi, and Armando Acosta. "Role of Interferons in the Development of Diagnostics, Vaccines, and Therapy for Tuberculosis." Journal of Immunology Research 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/5212910.

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Tuberculosis (TB) is an airborne infection caused byMycobacterium tuberculosis(Mtb). About one-third of the world’s population is latently infected with TB and 5–15% of them will develop active TB in their lifetime. It is estimated that each case of active TB may cause 10–20 new infections. Host immune response to Mtb is influenced by interferon- (IFN-) signaling pathways, particularly by type I and type II interferons (IFNs). The latter that consists of IFN-γhas been associated with the promotion of Th1 immune response which is associated with protection against TB. Although this aspect remai

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13

Fenton, Sarah E., Diana Saleiro, and Leonidas C. Platanias. "Type I and II Interferons in the Anti-Tumor Immune Response." Cancers 13, no. 5 (2021): 1037. http://dx.doi.org/10.3390/cancers13051037.

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The interferons (IFNs) are essential components of the immune response against infections and malignancies. IFNs are potent promoters of the anti-tumor response, but there is also evidence that feedback mechanisms regulated by IFNs negatively control immune responses to avoid hyper-activation and limit inflammation. This balance of responses plays an important role in cancer surveillance, immunoediting and response to anticancer therapeutic approaches. Here we review the roles of both type I and type II IFNs on the control of the immune response against malignancies in the context of effects o

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Ershov, F. I., and A. N. Narovlyansky. "The problem of the use of interferons in the novel coronavirus disease COVID-19 (Coronaviridae: Coronavirinae: Betacoronavirus: Sarbecovirus)." Problems of Virology 67, no. 2 (2022): 115–25. http://dx.doi.org/10.36233/0507-4088-103.

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By the end of 2021, about 200 studies on the effect of interferons (IFNs) on the incidence and course of the new coronavirus infection COVID-19 (Coronaviridae: Coronavirinae: Betacoronavirus: Sarbecovirus) have been reported worldwide, with the number of such studies steadily increasing. This review discusses the main issues of the use of IFN drugs in this disease. The literature search was carried out in the PubMed, Scopus, Cochrane Library, Web of Science, RSCI databases, as well as in the Google Scholar preprint database using the available search queries «MeSH for coronavirus», «SARS-CoV-2

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15

Xu, Renhuan, and Luis Sigal. "Antibody-blockade of a Type I interferon receptor decoy cures a viral disease by restoring liver interferon signaling (106.27)." Journal of Immunology 186, no. 1_Supplement (2011): 106.27. http://dx.doi.org/10.4049/jimmunol.186.supp.106.27.

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Abstract Type 1 interferons (T1-IFNs) play a major role in antiviral defense. Orthopoxviruses, including those that produce smallpox and mousepox encode a decoy receptor for T1-IFN, the T1-IFN binding protein (T1-IFNbp), which is essential for virulence. We demonstrate that during mousepox, T1-IFNs protects locally in the liver rather than systemically, and that the T1-IFNbp attaches to uninfected cells surrounding infectious foci in the liver to impair their ability to signal interferon, thus facilitating virus spread. Remarkably, this process can be reverted late in infection by treating wit

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16

Tuttle, Kathryn, Katherine A. Waugh, Ross Minter, Kelly D. Sullivan, and Joaquin M. Espinosa. "Defining the role of interferon signaling in mouse models of Down syndrome." Journal of Immunology 202, no. 1_Supplement (2019): 181.10. http://dx.doi.org/10.4049/jimmunol.202.supp.181.10.

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Abstract Down syndrome (DS) is caused by triplication of chromosome 21 (chr21) and is the most common chromosomal abnormality (1/700 live births). Our lab recently identified interferons (IFNs) as a core signaling pathway hyperactivated among diverse lineages of primary immune cells from individuals with DS. Notably, four of the six IFN receptor (IFNR) subunits for Types I, II, and III IFNs are encoded on chr21. Heightened IFN signaling in the disomic population is associated with developmental defects, cognitive impairments, and autoimmunity, a clinical profile highly similar to individuals w

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17

Oliveira, Danilo Bretas de, Gabriel Magno de Freitas Almeida, Antônio Carlos Martins Guedes, et al. "Basal Activation of Type I Interferons (Alpha2 and Beta) and2′5′OAS Genes: Insights into Differential Expression Profiles of Interferon System Components in Systemic Sclerosis." International Journal of Rheumatology 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/275617.

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Objective. Systemic sclerosis (SSc) is a complex autoimmune disease in which interferons (IFNs) may play an essential role. We hypothesized that type I and III IFNs may be found in increased levels in patients and be responsible for SSc autoimmune status.Methods. Type I and III IFN and ISG basal expression profiles were measured by qPCR using RNA from PBMCs of patients and controls .Results. Type I IFNs are increased in SSc patients, while no induction of type III IFNs was detected. This induction cannot be related to IRF7, since no upregulation of this gene was seen on patients. Of the ISGs t

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Malik, Aniko E., Thomas B. Issekutz, and Beata Derfalvi. "The Role of Type III Interferons in Human Disease." Clinical and Investigative Medicine 44, no. 2 (2021): E5–18. http://dx.doi.org/10.25011/cim.v44i2.36622.

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Purpose: This literature review summarizes the main immunological characteristics of type III interferons (IFN) and highlights the clinically relevant aspects and future therapeutic perspectives for these inflammatory molecules.  Source: Relevant articles in PubMed MEDLINE from the first publication (2003) until 2020. N=101 articles were included in this review.  Principal findings: Type III IFNs represent a relatively newly described inflammatory cytokine family. Although they induce substantially similar signalling to the well-known type I IFNs, significant functional

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19

Stone, Virginia M., Emma E. Ringqvist, Pär G. Larsson, et al. "Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection?" Microorganisms 9, no. 1 (2021): 105. http://dx.doi.org/10.3390/microorganisms9010105.

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Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFNλs; IL-28A, IL-28B, IL29, and IFNλ4) in the intestine. However, many viruses have developed strategies to counteract these defense mechanisms by preventing the production of IFNs. Here we use infection models, a clinical virus isolate, and several molecular biology techniques to demonstrate that both type I and III IFNs induce an antiviral state and attenuate Coxsackievirus group B (CVB) replication in human intestinal epithelial cells (IECs). While treatment of IECs with a viral mimic (po

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20

Onsa-Ard, Amnart, Rungthip Thongboontho, Narongsuk Munkong, et al. "Anti-Inflammatory Effects of Red Rice Bran Extract Ameliorate Type I Interferon Production via STING Pathway." Foods 11, no. 11 (2022): 1622. http://dx.doi.org/10.3390/foods11111622.

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Type I interferons (IFNs-I) are inflammatory cytokines that play an essential role in the pathogenesis of inflammation and autoimmune diseases. Signaling through nucleic acid sensors causes the production of IFNs-I. A stimulator of interferon genes (STING) is a DNA sensor that signals transduction, leading to the production of IFNs-I after their activation. This study aims to determine the anti-inflammatory effects of red rice bran extract (RRBE) on macrophages through the activation of STING signaling. RAW264.7 macrophage cells were stimulated with STING agonist (DMXAA) with and without RRBE.

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Kisand, Kai, Maire Link, Anette S. B. Wolff, et al. "Interferon autoantibodies associated with AIRE deficiency decrease the expression of IFN-stimulated genes." Blood 112, no. 7 (2008): 2657–66. http://dx.doi.org/10.1182/blood-2008-03-144634.

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Abstract Neutralizing autoantibodies to type I, but not type II, interferons (IFNs) are found at high titers in almost every patient with autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED), a disease caused by AIRE gene mutations that lead to defects in thymic T-cell selection. Combining genome-wide expression array with real time RT-PCR assays, we here demonstrate that antibodies against IFN-α cause highly significant down-regulation of interferon-stimulated gene expression in cells from APECED patients' blood by blocking their highly dilute endogenous IFNs. This down-reg

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Quesada, J. R., M. Talpaz, A. Rios, R. Kurzrock, and J. U. Gutterman. "Clinical toxicity of interferons in cancer patients: a review." Journal of Clinical Oncology 4, no. 2 (1986): 234–43. http://dx.doi.org/10.1200/jco.1986.4.2.234.

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All major types of human interferons (IFNs) have been purified and clinically administered as antitumor agents. We summarize here experience to date with toxicity of IFNs in cancer patients. The acute syndrome consists of fever, chills, myalgias, arthralgias, and headache, with some variation according to type of IFN, route of administration, schedule, and dose. Fatigue, perhaps reflecting CNS toxicity, is the most prevalent nonacute symptom. At high doses, IFNs are neurotoxic; the abnormalities seen by EEG resemble those in diffuse encephalitis. Hematologic toxicity consists mainly of leukope

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Kotenko, Sergei V., and Joan E. Durbin. "Contribution of type III interferons to antiviral immunity: location, location, location." Journal of Biological Chemistry 292, no. 18 (2017): 7295–303. http://dx.doi.org/10.1074/jbc.r117.777102.

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Type I interferons (IFN-α/β) and the more recently identified type III IFNs (IFN-λ) function as the first line of defense against virus infection and regulate the development of both innate and adaptive immune responses. Type III IFNs were originally identified as a novel ligand-receptor system acting in parallel with type I IFNs, but subsequent studies have provided increasing evidence for distinct roles for each IFN family. In addition to their compartmentalized antiviral actions, these two systems appear to have multiple levels of cross-regulation and act coordinately to achieve effective a

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Tsoncheva, Vania L., Kristina A. Todorova, and Vera A. Maximova. "Decreased DNA Repair Capacity of UV-Irradiated Cells Following Interferon Treatment." Zeitschrift für Naturforschung C 63, no. 7-8 (2008): 605–11. http://dx.doi.org/10.1515/znc-2008-7-823.

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The aim of this study was to examine the effect of interferons (IFNs) on the recovery of UV-damaged cells by means of measuring cell viability rates. The influence of the recombinant human interferons IFN-α, IFN-βand IFN-γ on the repair capacity of the UV-irradiated human cell lines WISH and HeLa was studied. The ability of cells to repair UV-induced damage was determined by the comet assay and both short- and long-term survival assays in proliferating cell cultures. We found that INFs negatively regulated DNA repair in cells damaged by UV light. One day after treatment, in both cell lines tes

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Utay, Netanya Sandler, and Daniel C. Douek. "Interferons and HIV Infection: The Good, the Bad, and the Ugly." Pathogens and Immunity 1, no. 1 (2016): 107. http://dx.doi.org/10.20411/pai.v1i1.125.

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Whether type I interferons (IFNs) hinder or facilitate HIV disease progression is controversial. Type I IFNs induce the production of restriction factors that protect against mucosal HIV/SIV acquisition and limit virus replication once systemic infection is established. However, type I IFNs also increase systemic immune activation, a predictor of poor CD4+ T-cell recovery and progression to AIDS, and facilitate production and recruitment of target CD4+ T cells. In addition, type I IFNs induce CD4+ T-cell apoptosis and limit antigen-specific CD4+ and CD8+ T-cell responses. The outcomes of type

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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.

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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

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Tan, Ping-Heng, Jasmine Ji, Chung-Hsi Hsing, Radika Tan, and Ru-Rong Ji. "Emerging Roles of Type-I Interferons in Neuroinflammation, Neurological Diseases, and Long-Haul COVID." International Journal of Molecular Sciences 23, no. 22 (2022): 14394. http://dx.doi.org/10.3390/ijms232214394.

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Interferons (IFNs) are pleiotropic cytokines originally identified for their antiviral activity. IFN-α and IFN-β are both type I IFNs that have been used to treat neurological diseases such as multiple sclerosis. Microglia, astrocytes, as well as neurons in the central and peripheral nervous systems, including spinal cord neurons and dorsal root ganglion neurons, express type I IFN receptors (IFNARs). Type I IFNs play an active role in regulating cognition, aging, depression, and neurodegenerative diseases. Notably, by suppressing neuronal activity and synaptic transmission, IFN-α and IFN-β pr

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Chandrasekaran, Sanjay, Maiko Sasaki, and Brian Paul Pollack. "PTEN/PI3K signaling in cancer and the response to cytokines: From growth factors to immune actors." Journal of Clinical Oncology 37, no. 8_suppl (2019): 35. http://dx.doi.org/10.1200/jco.2019.37.8_suppl.35.

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35 Background: The PTEN/PIK3 pathway plays an important role in the cellular response to growth factors and aberrant activation of PI3K signaling is a hallmark of many forms of cancer. While the role of PI3K signaling has been well studied in the context of growth factor biology, its role in the cellular response to cytokines such as interferons (IFNs) is less well understood. We examined the impact of PI3K activation on interferon signaling pathways using an in vitro experimental model system. Methods: Cultured human HCT 116 colorectal carcinoma cells and isogenic PTEN (-/-) cells were treate

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Leib, David A., Travis E. Harrison, Kathleen M. Laslo, Michael A. Machalek, Nathaniel J. Moorman, and Herbert W. Virgin. "Interferons Regulate the Phenotype of Wild-type and Mutant Herpes Simplex Viruses In Vivo." Journal of Experimental Medicine 189, no. 4 (1999): 663–72. http://dx.doi.org/10.1084/jem.189.4.663.

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Mechanisms responsible for neuroattenuation of herpes simplex virus (HSV) have been defined previously by studies of mutant viruses in cultured cells. The hypothesis that null mutations in host genes can override the attenuated phenotype of null mutations in certain viral genes was tested. Mutants such as those in infected cell protein (ICP) 0, thymidine kinase, ribonucleotide reductase, virion host shutoff, and ICP34.5 are reduced in their capacity to replicate in nondividing cells in culture and in vivo. The replication of these viruses was examined in eyes and trigeminal ganglia for 1–7 d a

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Liu, Ming-Liang, Yi-Ping Lee, Ya-Fang Wang, et al. "Type I interferons protect mice against enterovirus 71 infection." Journal of General Virology 86, no. 12 (2005): 3263–69. http://dx.doi.org/10.1099/vir.0.81195-0.

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In this study, the contribution of type I interferons (IFNs) to protection against infection with enterovirus 71 (EV71) was investigated using a murine model where the virus was administrated to neonatal Institute of Cancer Research (ICR) mice by either the intraperitoneal (i.p.) or the oral route. In i.p. inoculated mice, post-infection treatment of dexamethasone (5 mg kg−1 at 2 or 3 days after infection) exacerbated clinical symptoms and increased the tissue viral titre. In contrast, polyriboinosinic : polyribocytidylic acid [poly(I : C); 10 or 100 μg per mouse at 12 h before infection], a p

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Li, Shi-fang, Mei-jiao Gong, Fu-rong Zhao, et al. "Type I Interferons: Distinct Biological Activities and Current Applications for Viral Infection." Cellular Physiology and Biochemistry 51, no. 5 (2018): 2377–96. http://dx.doi.org/10.1159/000495897.

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The interferons (IFNs) are a primary defense against pathogens because of the strong antiviral activities they induce. IFNs can be classified into three groups: type I, type II and type III, according to their genetic, structural, and functional characteristics and their receptors on the cell surface. The type I IFNs are the largest group and include IFN-α, IFN-β, IFN-ε, IFN-ω, IFN-κ, IFN-δ, IFN-τ and IFN-ζ. The use of IFNs for the treatment of viral infectious diseases on their antiviral activity may become an important therapeutic option, for example, IFN-α is well known for the successful t

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Liu, Qizhi, Youliang Rao, Mao Tian, Shu Zhang, and Pinghui Feng. "Modulation of Innate Immune Signaling Pathways by Herpesviruses." Viruses 11, no. 6 (2019): 572. http://dx.doi.org/10.3390/v11060572.

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Herpesviruses can be detected by pattern recognition receptors (PRRs), which then activate downstream adaptors, kinases and transcription factors (TFs) to induce the expression of interferons (IFNs) and inflammatory cytokines. IFNs further activate the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, inducing the expression of interferon-stimulated genes (ISGs). These signaling events constitute host innate immunity to defeat herpesvirus infection and replication. A hallmark of all herpesviruses is their ability to establish persistent infection in the presence

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Gallagher, Grant, Rachael Siegel, and Joyce Eskdale. "Regulation of type-III interferons in airway epithelial cells. (51.13)." Journal of Immunology 184, no. 1_Supplement (2010): 51.13. http://dx.doi.org/10.4049/jimmunol.184.supp.51.13.

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Abstract The type-III interferons (IFNs) are the most recently discovered IFN family, comprising three protein ligands: IFN-λ1, IFN-λ2 and IFN-λ3. Their expression is induced by viruses and they share many anti-viral characteristics with the type-I IFNs (IFN-α and IFN-β), but type-III IFNs have an important specific functional niche at the immune-epithelial interface. However, their expression is diminished in bronchial epithelial cells of rhinovirus-infected asthmatic individuals. We set out to understand type-III IFN regulation. Here, we identify critical elements for IFN-λ1 promoter regulat

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Stephens, Laura M., and Steven M. Varga. "Function and Modulation of Type I Interferons during Respiratory Syncytial Virus Infection." Vaccines 8, no. 2 (2020): 177. http://dx.doi.org/10.3390/vaccines8020177.

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Respiratory syncytial virus (RSV) is the leading cause of lower respiratory infections in infants and young children, accounting for an estimated 3 million hospitalizations annually worldwide. Despite the major health burden, there is currently no licensed RSV vaccine. RSV is recognized by a range of cellular receptors including both toll-like receptors (TLR) and retinoic acid-inducible gene-I-like receptors (RIG-I). This interaction initiates signaling through mitochondrial antiviral signaling (MAVS) and interferon regulatory factor (IRF) proteins, resulting in the induction of type I interfe

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Khan, O. A., H. Jiang, P. S. Subramaniam, H. M. Johnson, and S. S. Dhib-Jalbut. "Immunomodulating functions of recombinant ovine interferon tau: potential for therapy in mulitple sclerosis and autoimmune disorders." Multiple Sclerosis Journal 4, no. 2 (1998): 63–69. http://dx.doi.org/10.1177/135245859800400204.

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The interferons (IFN) are a family of complex proteins possessing antiviral, antiproliferative, and immunomodulatory activities. Two type 1 recombinant human IFN have been recently approved for the treatment of multiple sclerosis (MS). However, use of high dose type 1 IFN treatment in MS patients has been limited by dose-related toxicity. Ovine IFNt is a unique type 1 interferon discovered for its role in the animal reproductive cycle. It differs from other type 1 IFNs in that it is remarkably less toxic even at high concentrations, is able to cross species barriers, and is not inducible by vi

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Zhou, Jian-hua, Yi-ning Wang, Qiu-yan Chang, Peng Ma, Yonghao Hu, and Xin Cao. "Type III Interferons in Viral Infection and Antiviral Immunity." Cellular Physiology and Biochemistry 51, no. 1 (2018): 173–85. http://dx.doi.org/10.1159/000495172.

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Interferons (IFNs) can serve as the first line of immune defense against viral infection. The identification of IFN-λs 1, 2, 3 & 4 (termed as type III IFNs) has revealed that the antiviral immune response to viruses contains more components than the type I IFNs that have been known for more than 50 years. IFN-λs are IFN-λ1 (IL-29), IFN-λ2 (IL-28a), IFN-λ3 (IL-28b) and IFN-λ4, which resembles IFN-λ3. IFN-λs have type I-IFN-like immune responses and biological activities, but our knowledge of these novel players in the antiviral response is not well established. In this review, we try to des

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Liu, Wenli, and Griffin P. Rodgers. "Upregulation of hGC-1 Expression by Hypomethylation, Retinoic Acid and Interferons in Human Myeloid Leukemia." Blood 112, no. 11 (2008): 4486. http://dx.doi.org/10.1182/blood.v112.11.4486.4486.

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Abstract hGC-1 (Granulocyte colony stimulating factor induced gene-1, also called GW112 and olfactomedin 4) was first identified in human myeloid precursor cells induced by granulocyte colony stimulating factor (G-CSF). It is a myeloid lineage and differentiation stage specific gene. Its expression, regulation and biological function, specifically in myeloid cells, are still poorly understood. In this study, we analyzed the hGC-1 gene expression in leukemia patients and further investigated the mechanism of hGC-1 gene regulation in leukemia cells. We found that hGC-1 was overexpressed in myelo

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Sim, Tao Ming, Siying Jane Ong, Anselm Mak, and Sen Hee Tay. "Type I Interferons in Systemic Lupus Erythematosus: A Journey from Bench to Bedside." International Journal of Molecular Sciences 23, no. 5 (2022): 2505. http://dx.doi.org/10.3390/ijms23052505.

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Dysregulation of type I interferons (IFNs) has been implicated in the pathogenesis of systemic lupus erythematosus (SLE) since the late 1970s. The majority of SLE patients demonstrate evidence of type I IFN pathway activation; however, studies attempting to address the relationship between type I IFN signature and SLE disease activity have yielded conflicting results. In addition to type I IFNs, type II and III IFNs may overlap and also contribute to the IFN signature. Different genetic backgrounds lead to overproduction of type I IFNs in SLE and contribute to the breakdown of peripheral toler

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Takahashi, Shinichiro. "Kinase Inhibitors and Interferons as Other Myeloid Differentiation Inducers in Leukemia Therapy." Acta Haematologica 145, no. 2 (2021): 113–21. http://dx.doi.org/10.1159/000519769.

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Differentiation therapy using all-<i>trans</i> retinoic acid (ATRA) is well established for the treatment of acute promyelocytic leukemia (APL). Several attempts have been made to treat non-APL acute myeloid leukemia (AML) patients by employing differentiation inducers, such as hypomethylating agents and low-dose cytarabine, with encouraging results. In the present review, I focus on other possible differentiation inducers: kinase inhibitors and interferons (IFNs). A number of kinase inhibitors have been reported to induce differentiation, including CDK inhibitors, GSK3 inhibitors,

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Stanifer, Megan L., Kalliopi Pervolaraki, and Steeve Boulant. "Differential Regulation of Type I and Type III Interferon Signaling." International Journal of Molecular Sciences 20, no. 6 (2019): 1445. http://dx.doi.org/10.3390/ijms20061445.

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Interferons (IFNs) are very powerful cytokines, which play a key role in combatting pathogen infections by controlling inflammation and immune response by directly inducing anti-pathogen molecular countermeasures. There are three classes of IFNs: type I, type II and type III. While type II IFN is specific for immune cells, type I and III IFNs are expressed by both immune and tissue specific cells. Unlike type I IFNs, type III IFNs have a unique tropism where their signaling and functions are mostly restricted to epithelial cells. As such, this class of IFN has recently emerged as a key player

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Chessler, Anne-Danielle C., Kacey L. Caradonna, Akram Da'dara, and Barbara A. Burleigh. "Type I Interferons Increase Host Susceptibility to Trypanosoma cruzi Infection." Infection and Immunity 79, no. 5 (2011): 2112–19. http://dx.doi.org/10.1128/iai.01176-10.

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ABSTRACTTrypanosoma cruzi, the protozoan parasite that causes human Chagas' disease, induces a type I interferon (IFN) (IFN-α/β) response during acute experimental infection in mice and in isolated primary cell types. To examine the potential impact of the type I IFN response in shaping outcomes in experimentalT. cruziinfection, groups of wild-type (WT) and type I IFN receptor-deficient (IFNAR−/−) 129sv/ev mice were infected with two differentT. cruzistrains under lethal and sublethal conditions and several parameters were measured during the acute stage of infection. The results demonstrate t

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Sauer, John-Demian, Katia Sotelo-Troha, Jakob von Moltke, et al. "TheN-Ethyl-N-Nitrosourea-InducedGoldenticketMouse Mutant Reveals an Essential Function ofStingin theIn VivoInterferon Response toListeria monocytogenesand Cyclic Dinucleotides." Infection and Immunity 79, no. 2 (2010): 688–94. http://dx.doi.org/10.1128/iai.00999-10.

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ABSTRACTType I interferons (IFNs) are central regulators of the innate and adaptive immune responses to viral and bacterial infections. Type I IFNs are induced upon cytosolic detection of microbial nucleic acids, including DNA, RNA, and the bacterial second messenger cyclic-di-GMP (c-di-GMP). In addition, a recent study demonstrated that the intracellular bacterial pathogenListeria monocytogenesstimulates a type I IFN response due to cytosolic detection of bacterially secreted c-di-AMP. The transmembrane signaling adaptor Sting (Tmem173, Mita, Mpys, Eris) has recently been implicated in the in

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Doughty, Lesley, Vivian Wolfe, Basilia Zingarelli та Hector Wong. "INTERFERONS (IFNS) PROLONG LPS ACTIVATION OF THE NFκB PATHWAY." Critical Care Medicine 34 (грудень 2006): A33. http://dx.doi.org/10.1097/00003246-200612002-00115.

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Borden, Ernest C., Dan L. Lindner, and Edward Schwartz. "Increasing interferons (IFNs) effectiveness through augmentation of gene expression." European Journal of Cancer 33 (June 1997): S11. http://dx.doi.org/10.1016/s0959-8049(97)89356-2.

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Barrales-Cureño, Hebert Jair, César Reyes-Reyes, Maximino Diaz-Bautista, Adrián Gómez-de Jesús, Salvador Chávez-Salinas, and Luis Germán López-Valdez. "Therapeutic effects of interferons in human viral infections." Mexican Journal of Biotechnology 3, no. 4 (2018): 19–32. http://dx.doi.org/10.29267/mxjb.2018.3.4.19.

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The interferon (IFN) is a cytokine produced by immunocompetent cells in response to various stimuli. Five types of IFNs are identified: alpha, beta, gamma, tau and omega 1. In particular, interferons inhibit viral replication directly by antiviral mechanisms, as they do so indirectly by amplifying immune responses to viral proteins. Likewise, they are also essential elements in clinical oncology. They are used in the treatment of chronic myelocytic and hairy cell leukemia, multiple myeloma, non-Hodgkin's lymphoma, melanoma, renal carcinoma, and Kaposi's sarcoma, as well as in the papilloma. Th

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Zhang, Yubin, Vinh Thai, Amanda McCabe, Maura Jones, and Katherine C. MacNamara. "Type I Interferons Promote Severe Disease in a Mouse Model of Lethal Ehrlichiosis." Infection and Immunity 82, no. 4 (2014): 1698–709. http://dx.doi.org/10.1128/iai.01564-13.

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ABSTRACTHuman monocytic ehrlichiosis (HME) is caused by a tick-borne obligate intracellular pathogen of the orderRickettsiales. HME disease can range from mild to a fatal, toxic shock-like syndrome, yet the mechanisms regulating pathogenesis are not well understood. We define a central role for type I interferons (alpha interferon [IFN-α] and IFN-β) in severe disease in a mouse model of fatal ehrlichiosis caused byIxodes ovatusEhrlichia(IOE). IFN-α and IFN-β were induced by IOE infection but not in response to a less virulent strain,Ehrlichia muris. The major sources of type I IFNs during IOE

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Bartlett, Nathan W., Karen Buttigieg, Sergei V. Kotenko, and Geoffrey L. Smith. "Murine interferon lambdas (type III interferons) exhibit potent antiviral activity in vivo in a poxvirus infection model." Journal of General Virology 86, no. 6 (2005): 1589–96. http://dx.doi.org/10.1099/vir.0.80904-0.

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Human interferon lambdas (IFN-λs) (type III IFNs) exhibit antiviral activity in vitro by binding to a receptor complex distinct from that used by type I and type II IFNs, and subsequent signalling through the Janus kinase signal transducers and activators of transcription (STAT) pathway. However, evidence for a function of type III IFNs during virus infection in vivo is lacking. Here, the expression of murine IFN-λs by recombinant vaccinia virus (VACV) is described and these proteins are shown to have potent antiviral activity in vivo. VACV expressing murine IFN-λ2 (vIFN-λ2) and IFN-λ3 (vIFN-λ

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Onabajo, Olusegun O., Nina Rao, Adeola A. Obajemu та ін. "IFN-λ4 induces a faster but more transient antiviral response compared to other type III interferons". Journal of Immunology 198, № 1_Supplement (2017): 158.13. http://dx.doi.org/10.4049/jimmunol.198.supp.158.13.

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Abstract IFN-λ4, a recently discovered type-III interferon (IFN), is genetically regulated, and has clinical significance because of its association with impaired clearance of hepatitis C virus (HCV) infection. Type-III IFNs play a critical role in the innate immune response to viral infections. Although IFN-λ4 induces a similar antiviral profile as other type-III IFNs, its specific contribution to the innate immune response is unclear. Delineating the functional properties of IFN-λ4 that distinguish it from other type-III IFNs may give insights into its unique role during HCV, and other infec

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Melchjorsen, Jesper, Johanna Rintahaka, Stine Søby, et al. "Early Innate Recognition of Herpes Simplex Virus in Human Primary Macrophages Is Mediated via the MDA5/MAVS-Dependent and MDA5/MAVS/RNA Polymerase III-Independent Pathways." Journal of Virology 84, no. 21 (2010): 11350–58. http://dx.doi.org/10.1128/jvi.01106-10.

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ABSTRACT Innate recognition of viruses is mediated by pattern recognition receptors (PRRs) triggering expression of antiviral interferons (IFNs) and proinflammatory cytokines. In mice, Toll-like receptor 2 (TLR2) and TLR9 as well as intracellular nucleotide-sensing pathways have been shown to recognize herpes simplex virus (HSV). Here, we describe how human primary macrophages recognize early HSV infection via intracellular pathways. A number of inflammatory cytokines, IFNs, and IFN-stimulated genes were upregulated after HSV infection. We show that early recognition of HSV and induction of IF

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Snyder, Deann T., Jodi F. Hedges, and Mark A. Jutila. "Getting “Inside” Type I IFNs: Type I IFNs in Intracellular Bacterial Infections." Journal of Immunology Research 2017 (2017): 1–17. http://dx.doi.org/10.1155/2017/9361802.

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Type I interferons represent a unique and complex group of cytokines, serving many purposes during innate and adaptive immunity. Discovered in the context of viral infections, type I IFNs are now known to have myriad effects in infectious and autoimmune disease settings. Type I IFN signaling during bacterial infections is dependent on many factors including whether the infecting bacterium is intracellular or extracellular, as different signaling pathways are activated. As such, the repercussions of type I IFN induction can positively or negatively impact the disease outcome. This review focuse

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