Relevant bibliographies by topics / INTERFERON SIGNATURE

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'INTERFERON SIGNATURE'

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Published: 1 April 2023

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Journal articles on the topic "INTERFERON SIGNATURE"

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Visan, Ioana. "The interferon signature." Nature Immunology 18, no. 2 (February 2017): 151. http://dx.doi.org/10.1038/ni.3670.

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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 (May 23, 2021): 279–84. http://dx.doi.org/10.51620/0869-2084-2021-66-5-279-284.

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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 IFN1 pathway is known as interferon score. This review discusses the possible causes of upregulated expression of interferon 1-induced genes, the laboratory approaches to the interferon score analysis, as well as the practical use of this indicator for the diagnosis of various conditions.
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Smith, Michael Alexander, Chia-Chien Chiang, Dominic Sinibaldi, Kamelia Zerrouki, Zerai Manna, Wendy I. White, Mariana J. Kaplan, et al. "Using the Circulating Proteome to Assess Type I Interferon Activity in Systemic Lupus Erythematosus." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 210.1. http://dx.doi.org/10.4049/jimmunol.198.supp.210.1.

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Abstract Type I interferon (IFN) signaling drives pathology in systemic lupus erythematosus (SLE) and can be tracked via IFN-inducible transcripts present in whole blood as described by several IFN gene signatures. As SLE is a complex disease affecting diverse organ systems, we examined whether measurement of circulating proteins, which can infiltrate the bloodstream from afflicted tissues, might also offer insight into global IFN activity. The presence of anti-DNA autoantibodies in patient serum has prevented effective use of SOMAmers for the evaluation of circulating proteins in SLE. Here, we adapted protocols to mitigate for those autoantibodies and report high reproducibility and accuracy with 100% QC pass rate and improved correlation with previously validated multi-analyte platform results. Using SOMAmers together with the IFN 21-gene signature1 (IFNGS), we derived an IFN protein signature that can approximate the IFNGS score. In a cohort of 82 SLE patients and 48 healthy donors, the protein signature was found elevated above healthy donors for most of IFNGS-high patients (49/55, 89%) and also for a subgroup of IFNGS-low patients (7/27, 26%). The protein signature correlated with global disease activity (median SLEDAI score of 4 for the cohort) in both lymphopenic and non-lymphopenic patients. Significant associations with skin involvement, low complement, anti DNA auto-antibodies, and thrombocytopenia were also observed. In sum, our results suggest blood derived protein measurements may complement validated gene signatures to monitor IFN activity.
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Rigolet, Muriel, Cyrielle Hou, Yasmine Baba Amer, Jessie Aouizerate, Baptiste Periou, Romain K. Gherardi, Peggy Lafuste, and François Jérôme Authier. "Distinct interferon signatures stratify inflammatory and dysimmune myopathies." RMD Open 5, no. 1 (February 2019): e000811. http://dx.doi.org/10.1136/rmdopen-2018-000811.

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ObjectiveThe role of interferons (IFN) in the pathophysiology of primary inflammatory and dysimmune myopathies (IDM) is increasingly investigated, notably because specific neutralisation approaches may constitute promising therapeutic tracks. In present work we analysed the muscular expression of specific IFNα/β and IFNγ-stimulated genes in patients with various types of IDM.Methods39 patients with IDM with inclusion body myositis (IBM, n=9), dermatomyositis (DM, n=10), necrotising autoimmune myopathies (NAM, n=10) and antisynthetase myositis (ASM, n=10), and 10 controls were included. Quantification of expression levels of IFNγ, ISG15, an IFNα/β-inducible gene and of six IFNγ-inducible genes (GBP2, HLA-DOB, HLA-DPB, CIITA, HLA-DRB and HLA-DMB) was performed on muscle biopsy samples.ResultsDM usually associated with strong type I IFNα/β signature, IBM and ASM with prominent type II IFNγ signature and NAM with neither type I nor type II IFN signature. Immunofluorescence study in ASM and IBM showed myofibre expression of major histocompatibility class 2 (MHC-2) and CIITA, confirming the induction of the IFNγ pathway. Furthermore, MHC-2-positive myofibres were observed in close proximity to CD8+ T cells which produce high levels of IFNγ.ConclusionDistinct IFN signatures allow a more distinct segregation of IDMs and myofibre MHC-2 expression is a reliable biomarker of type II IFN signature.
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Carrero, Javier, Boris Calderon, Stephen Ferris, and Emil Unanue. "Evaluation of the role of type I interferon to the development of type 1 diabetes. (BA3P.131)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 44.1. http://dx.doi.org/10.4049/jimmunol.192.supp.44.1.

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Abstract Our goal is to identify the earliest immunologically relevant events that trigger autoimmune diabetes. The first detectable inflammatory signature in the NOD mouse is the upregulation of type I interferons and an interferon-inducible gene signature. We reason that understanding the early interferon signature may provide targets for the prevention, treatment, or diagnosis of autoimmune diabetes. The two ubiquitous interferon receptors (IFNAR and IFNGR) upregulate hundreds genes, some shared and some unique to each receptor. We backcrossed the type I interferon receptor onto NOD background to determine the relative contribution of IFNAR-inducible transcripts in type I diabetes induction. In our specific pathogen-free colony, NOD.IFNAR-/- mice developed diabetes at a decreased rate and penetrance from littermate controls. This reduction in incidence was gender independent and NOD.IFNAR heterozygous mice developed diabetes normally. There was a reduction in the number of the immunological infiltrates in the islets of Langerhans of NOD.IFNAR-/- mice from 4-8 wks of age as detected by flow cytometry and immunofluorescence. Concomitantly, there was a reduction in inflammatory gene expression in NOD.IFNAR-/- when compared to controls. Additionally, analysis of the NOD.IFNGR-/- mice showed a decrease in penetrance and kinetics of type I diabetes. Based on this data, we hypothesize that IFNAR and IFNGR induce a common genetic signature that is required for type I diabetes to proceed.
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An, Yuanyuan, and Hua Duan. "The Comprehensive Analysis of Interferon-Related Prognostic Signature with regard to Immune Features in Ovarian Cancer." Disease Markers 2022 (June 20, 2022): 1–24. http://dx.doi.org/10.1155/2022/7900785.

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Interferon plays an important role in immune response of ovarian cancer. However, the expression pattern of interferon in ovarian cancer remains unclear. This study is aimed at exploring the expression profile of interferon-relate genes and constructing an interferon-based prognostic signature in ovarian cancer. The ovarian cancer samples collected from TCGA database were viewed as the training set, and ovarian cancer samples collected from GEO datasets were used as the independent validation sets. Univariate Cox regression analysis and multivariate Cox regression analysis were used to construct interferon-related signature, which worked as independent prognostic factor. Bioinformatics based on David software, GSEA, and R software were used to investigate the relationship between immune status and the signature in ovarian cancer. The signature showed close correlation with the status for ovarian cancer immune microenvironment, which might provide the possibility for clinical targeted therapy.
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Gallay, Laure, Guy Mouchiroud, and Bénédicte Chazaud. "Interferon-signature in idiopathic inflammatory myopathies." Current Opinion in Rheumatology 31, no. 6 (November 2019): 634–42. http://dx.doi.org/10.1097/bor.0000000000000653.

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Rönnblom, Lars, and Maija-Leena Eloranta. "The interferon signature in autoimmune diseases." Current Opinion in Rheumatology 25, no. 2 (March 2013): 248–53. http://dx.doi.org/10.1097/bor.0b013e32835c7e32.

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Vieira, Matheus, Paul Régnier, Anna Maciejewski-Duval, Alexandre Le Joncour, Guillaume Darasse-Jèze, Michelle Rosenzwajg, David Klatzmann, Patrice Cacoub, and David Saadoun. "Interferon signature in giant cell arteritis aortitis." Journal of Autoimmunity 127 (February 2022): 102796. http://dx.doi.org/10.1016/j.jaut.2022.102796.

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Gruber, Conor. "Impaired interferon signature in severe COVID-19." Nature Reviews Immunology 20, no. 6 (April 30, 2020): 353. http://dx.doi.org/10.1038/s41577-020-0335-0.

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Dissertations / Theses on the topic "INTERFERON SIGNATURE"

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Lincez, Pamela Joan. "MDA5 and a type 1 interferon signature in the development of type 1 diabetes." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52850.

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Type 1 diabetes (T1D) is a debilitating disease involving the autoimmune destruction of insulin-producing pancreatic β-cells. The personal and economic burden of this disease is enormous, therefore simpler and more cost effective therapeutic approaches than those currently available must be explored. In children at risk for T1D, a unique type 1 interferon (IFN-I) transcriptional signature precedes islet autoimmunity. Recent onset of T1D strongly associates with infection by RNA viruses like coxsackievirus that induce IFN-I. Importantly, genetic variants in the T1D risk locus IFIH1 are linked to protection from T1D and result in reduced expression of the RNA virus sensor melanoma differentiation-associated protein 5 (MDA5), which is also a critical component in establishing the IFN-I signature. In chapter 2 we describe a novel model where we have translated the reduced MDA5 expression phenotype observed in patients onto the non-obese diabetic (NOD) mouse and established its importance in T1D. We describe the first observations that a reduction in MDA5 in the NOD mouse protects from spontaneous and coxsackievirus B4 (CB4)-induced T1D. We also establish the importance of a specific IFN-I signature in the development of T1D as a result of reduced (not eliminated) MDA5 sensing of CB4 that allows for regulatory T cells (Tregs) at the site of autoimmunity and protects from CB4 induced T1D. In chapter 3 we show that this unique IFN-I signature is limited to MDA5 and disease pathogenesis is linked to the specific IFN-I response induced by the virus as a strain of CB3 failed to modify the IFN-I signature associated with disease. Further RNA sequencing discussed in Chapter 4 demonstrates unique tissue-specific differential gene profiles associated with a reduction in MDA5 following CB4 infection. Our results support our hypothesis that there is a direct correlation between the IFN-I signature induced following environmental challenge with the induction of a strong effector T cell and a matched Treg response. This work demonstrates the essential role of MDA5 signaling in regulating the IFN-I signature, implicates MDA5 in T1D susceptibility and in protection against IFN-I and T1D-inducing agents like CB4 and suggests restricting MDA5 function as a potential T1D therapeutic.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Lisney, Anna [Verfasser]. "Analysis of SIGLEC1 as a surrogate marker for a type I interferon signature in autoimmune congenital heart block and primary Sjögren’s syndrome / Anna Lisney." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/120204381X/34.

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Domaszewska, Teresa. "Unraveling transcript-based variability of host responses to Tuberculosis." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/19829.

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Jedes Jahr treten weltweit über zehn Millionen Fälle von Tuberkulose (TB) auf. Die Weltgesundheitsorganisation (WHO) schätzt, dass ein Drittel der Weltbevölkerung mit dem Erreger Mycobacterium tuberculosis (Mtb) infiziert ist. Bei fünf bis zehn Prozent aller latent Infizierten bricht Tuberkulose im Laufe des Lebens aus. Dennoch sind bereits 100 Jahre seit der Entdeckung von Mtb vergangen, ohne dass die entscheidenden Faktoren für den unterschiedlichen Infektionsverlauf bekannt wären. In dieser Arbeit untersuche ich die unterschiedlichen Reaktionen auf eine Tuberkuloseinfektion in verschiedenen Wirten. In meinem ersten Ansatz habe ich öffentlich zugängliche Transkriptom-Datensätze von Tuberkulosepatienten und gesunden Probanden ausgewertet. Mit Hilfe der Gensatzanreicherungs-Analyse (eng. Gene Set Enrichment Analysis, GSEA) habe ich die Transkriptionsprofile von Tuberkulosepatienten betrachtet. Das besondere Augenmerk lag hierbei auf der Interferon (IFN)-Signalkaskade, die für den Krankheitsverlauf von besonderer Bedeutung ist. In dieser Arbeit zeige ich zunächst, dass Patienten ohne eine IFN-Signatur in der untersuchten Kohorte vorkommen und widme mich im Anschluss der Frage, ob diese Patienten einen anderen Phänotypus haben als jene mit einer starken IFN-Antwort. Indem ich nur Patienten ohne IFN-Antwort betrachte, werden Mechanismen deutlich, die allen Patientengruppen gemein sind, aber vorher von der starken IFN-Signatur überlagert wurden. Ich belege in dieser Arbeit, dass eine starke IFN-Regulation auch mit einer ausgeprägten Lungenpathologie in Tuberkulosepatienten einhergeht. Passend hierzu weisen auch gesunde Probanden nach Verabreichung des Impfstoffs FLUAD® einen erhöhten Blutwert IFN-induzierter Zytokine auf. Mit Hilfe maschinellen Lernens konnte ich Transkriptomsignaturen der Patienten mit bzw. ohne IFN-Antwort identifizieren und vergleichen. Im zweiten Ansatz widme ich mich den unterschiedlichen Transkriptionsantworten auf Mtb-Infektionen in humanen Kohorten und zwei verschiedenen Mausmodellen. Der humanen und der murinen Immunantwort auf Infektionen unterliegen gravierende Unterschiede. Trotzdem sind einige Elemente des Immunsystems in beiden Arten konserviert. In dieser Arbeit präsentiere ich einen neuen Ansatz der Datenintegration, der die Identifizierung von übereinstimmenden und nicht übereinstimmenden Regulationselementen der Genexpression in heterogenen Datensätzen ermöglicht. Die Analyse basiert auf öffentlich zugänglichen sowie de-novo-generierten Datensätzen, zu denen ich durch wissenschaftliche Kollaborationen meiner Kollegen in der Abteilung Immunologie sowie der zentralen Einheit Microarray des Max-Planck-Instituts für Infektionsbiologie, Zugang erhalten habe. Des Weiteren liegt ein Schwerpunkt auf der vergleichenden Analyse humaner und muriner Transkriptionsantworten auf Tuberkulose in Vollblut und Makrophagen. Die erhaltenen Ergebnisse weisen auf einen signifikanten Unterschied in der Regulierung der angeborenen sowie der erworbenen Immunität in Mensch und Maus als Reaktion auf eine Mtb-Infektion hin. In dieser Arbeit charakterisiere ich die unterschiedliche Regulierung von T-Zell bezogenen Genen, die mit unterschiedlich ausgeprägten Phänotypen bei stark oder schwach TB-anfälligen Mausstämmen korrespondiert. Darüber hinaus habe ich den 21. Tag nach einer Tuberkuloseinfektion in Mäusen als Zeitpunkt ermittelt, der die Transkriptionsantworten in den untersuchten humanen Kohorten am besten widerspiegelt. Die angewandten Ansätze erleichtern die Auswahl des am besten geeigneten Tiermodells für die Erforschung der humanen Immunantwort auf eine ausgewählte Krankheit und liefern die Basis für ein besseres Verständnis der unterschiedlichen Krankheitsverläufe in Mtb-infizierten Patienten.
Over 10 million tuberculosis (TB) cases are being reported annually and the World Health Organization (WHO) estimates that up to the 1/3 of the world population is infected with Mycobacterium tuberculosis (Mtb). Between 5 and 10% of the latently infected individuals develop TB during their lifetime. Yet, despite over 100 years of research since Mtb has been identified, we are not able to define all the factors which are responsible for the different infection outcomes in the hosts. In this thesis I investigate the variability in the response to TB presented by different hosts. In one approach, I collect publicly available transcriptomic datasets from TB patients and healthy donors. Using Gene Set Enrichment Analysis (GSEA) I examine transcriptional profiles of individuals with TB. In particular, focus is brought to interferon (IFN) signaling which has been previously described as crucial for the disease outcome. I show that patients lacking IFN signature are present in the studied cohorts and investigate whether these patients present different phenotype than patients with strong regulation of IFN responses. Moreover, by focusing on patients lacking IFN response I try to unearth mechanisms present in all patient groups but dominated by the signal of IFN response. I show that strong regulation of IFN genes is related to severe pathology in the lungs of TB patients and that it is reflected by the levels of IFN-inducible cytokines in blood of healthy volunteers after vaccination with FLUAD® vaccine. Using Machine Learning (ML) methods, I identify and compare transcriptomic signatures of the patients presenting and lacking the IFN response. In the second approach I study the differences in the transcriptional responses to Mtb infection in human cohorts and two different mouse models. The immunity in infection, inflammation and malignancy differs markedly in man and mouse. Nevertheless, there are elements of immune system which have been conserved between the species. I propose a novel data integration approach which identifies concordant and discordant elements of gene expression regulation in heterologous datasets. The analysis is based on publicly available as well as novel experimental data acquired thanks to collaboration with my colleagues from the Department of Immunology and Microarray Core Facility of Max Planck Institute for Infection Biology (MPIIB). Additionally, I focus on the comparison of human and murine transcriptional responses to TB in whole blood (WB) and in macrophages. The results indicate profound differences between regulation of innate and adaptive immunity in man and mouse upon Mtb infection. I characterize differential regulation of T-cell related genes corresponding to the differences in phenotype between TB high and low susceptible mouse strains and identify the time point of 21 days p.i. of mice as best reflection of transcriptional responses in the studied human cohorts. The implemented approaches facilitate the choice of an appropriate animal model for studies of the human immune response to a particular disease and provide the basis for better understanding of differences in the outcomes of Mtb infection in individual hosts.
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Strauß, Romy [Verfasser]. "Der Einfluss von Typ-I-Interferonen auf Leukozyten-Subpopulationen im Blut : ein neuer diagnostischer Ansatz für die Verwendung der Interferon-Signatur als Biomarker beim systemischen Lupus erythematodes / Romy Strauß." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1176632272/34.

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Imgenberg-Kreuz, Juliana. "Epigenetic and Gene Expression Signatures in Systemic Inflammatory Autoimmune Diseases." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-310388.

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Autoimmune diseases are clinical manifestations of a loss-of-tolerance of the immune system against the body’s own substances and healthy tissues. Primary Sjögren’s syndrome (pSS) and systemic lupus erythematosus (SLE) are two chronic inflammatory autoimmune diseases characterized by autoantibody production and an activated type I interferon system. Although the precise mechanisms leading to autoimmune processes are not well defined, recent studies suggest that aberrant DNA methylation and gene expression patterns may play a central role in the pathogenesis of these disorders. The aim of this thesis was to investigate DNA methylation and gene expression in pSS and SLE on a genome-wide scale to advance our understanding of how these factors contribute to the diseases and to identify potential biomarkers and novel treatment targets. In study I, differential DNA methylation was analyzed in multiple tissues from pSS patients and healthy controls. We identified thousands of CpG sites with perturbed methylation; the most prominent finding was a profound hypomethylation at regulatory regions of type I interferon induced genes in pSS. In study II, a cases-case study comparing DNA methylation in pSS patients with high fatigue to patients with low fatigue, we found methylation patterns associated to the degree of fatigue. In study III, RNA-sequencing was applied to investigate the transcriptome of B cells in pSS in comparison to controls. Increased expression of type I and type II interferon regulated genes in pSS was observed, indicating ongoing immune activation in B cells. In study IV, the impact of DNA methylation on disease susceptibility and phenotypic variability in SLE was investigated. We identified DNA methylation patterns associated to disease susceptibility, SLE manifestations and different treatments. In addition, we mapped methylation quantitative trait loci and observed evidence for genetic regulation of DNA methylation in SLE.   In conclusion, the results presented in this thesis provide new insights into the molecular mechanisms underlying autoimmunity in pSS and SLE. The studies confirm the central role of the interferon system in pSS and SLE and further suggest novel genes and mechanisms to be involved in the pathogenesis these autoimmune diseases.
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Outlioua, Ahmed. "Exploration des cytokines pro-inflammatoires et de l’inflammasome NLRP3 dans les infections intracellulaires : cas de H. pylori et des virus à ARN Gastric IL-1β, IL-8, and IL-17A expression in Moroccan patients infected with Helicobacter pylori may be a predictive signature of severe pathological stages RNA viruses promote activation of the NLRP3 inflammasome through cytopathogenic effect-induced potassium efflux The heme-regulated inhibitor is a cytosolic sensor of protein misfolding that controls innate immune signaling The Role of Optineurin in Antiviral Type I Interferon Production Possible introduction of Leishmania tropica to urban areas determined by epidemiological and clinical profiles of patients with cutaneous leishmaniasis in Casablanca (Morocco)." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL029.

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Helicobacter pylori (H. pylori) est une bactérie qui infecte l’estomac et induit une gastrite inflammatoire, qui peut être chronique et évoluer vers un cancer gastrique. La sévérité de l’infection et son évolution clinique sont associées aux différents facteurs notamment le statut immunitaire de l’hôte. La réponse inflammatoire initiale à l'infection à H. pylori entraîne la sécrétion d'un large panel de cytokines, notamment l'interleukine-1β (IL-1β), l'IL-8 et l'IL-17A. qui semblent jouer un rôle clé dans l'initiation et la progression du cancer gastrique. Parmi ces cytokines, l'IL-1β est une cytokine clé au cours de l’infection à H. pylori dont l’expression est étroitement associée à l'inflammation gastrique et à la carcinogenèse. La production de cette cytokine dépend de l'activation de l'inflammasome, en particulier l'inflammasome NLRP3. Ce dernier, responsable de l’activation des processus inflammatoires, est essentiel pour le maintien de l'homéostasie contre diverses infections pathogènes telles les infections bactérienne et virale.L’objectif général de ce travail est i) d’étudier l’expression et le polymorphisme des gènes de cytokines comme IL-1β, IL-17 et IL-8 chez des patients marocains infectés par H. pylori. ii) explorer l’activation de l'inflammasome NLRP3 par H. pylori et déterminer les mécanismes impliqués dans l'activation de ce complexe par des virus à ARN ; connus comme des activateurs définis de NLRP3.Nos résultats ont souligné une prévalence élevée de H. pylori et ont mis en évidence une signature cytokinique : elle peut prédire la métaplasie au cours de la progression de l'infection à H. pylori impliquant une diminution de l’expression de l'IL17A dans l’antre et une augmentation de l’expression de l'IL-1β dans le fundus. Plus particulièrement, les polymorphismes génétiques de l’IL-1β (IL-1β -31 et -511) ne semblent pas influencer l’expression de l’IL-1β de manière significative.Au regard des difficultés rencontrés pour l’isolement et la culture de H. pylori, nous avons utilisé le LPS de H. pylori pour stimuler l’inflammasome. Nos résultats montrent que la transfection des cellules in vitro par le LPS bactérien induit la production de l’IL-1β qui semble être modulée par la caspase 4, NOD1 et NOD2. Par ailleurs, bien qu’il soit clairement établi que les virus à ARN induisent l’activation de l’inflammasome NLRP3, les mécanismes par lesquels ces virus induisent la production d'IL-1β ne sont pas bien compris et restent à confirmer. Les résultats de cette partie du travail ont montré que la réplication des virus à ARN cytopathogènes tels que le virus de la stomatite vésiculaire (VSV) ou le virus de l'encéphalomyocardite (EMCV) induit une mort cellulaire lytique conduisant à un efflux de potassium qui déclenche l'activation de l'inflammasome NLRP3. Ainsi, les virus à forte capacité de réplication et qui ont un effet cytopathique sont capables d'induire l'activation de la caspase-1 conduisant à la production d'IL-1β. A l'inverse, les virus qui induisent une très bonne réponse IFN de type I sont de très mauvais inducteurs de l'inflammasome NLRP3.Une meilleure compréhension de l’activation de l’inflammasome pourrait aider dans la mise au point de stratégies thérapeutiques ciblées utilisables dans la lutte contre les infections bactérienne et virale.Mots clés : Helicobacter pylori, inflammation, inflammasome NLRP3, IL-1β, virus à ARN
Helicobacter pylori (H. pylori) is a bacteria that infects the stomach and induces inflammatory gastritis, which can be chronic and progress to gastric cancer. The severity of the infection and its clinical course are associated with various factors including the immune status of the host. The initial inflammatory response to H. pylori infection results in the secretion of a wide range of cytokines, including interleukin-1β (IL-1β), IL-8 and IL-17A. which appear to play a key role in the initiation and progression of gastric cancer. Among these cytokines, IL-1β is a key cytokine during H. pylori infection whose expression is associated with gastric inflammation and carcinogenesis. The production of this cytokine depends on the activation of the inflammasome, in particular the NLRP3 inflammasome. The latter, responsible of the activation of inflammatory processes, is essential for the maintenance of homeostasis against various pathogenic infections such as bacterial and viral infections.The general objective of this work is i) to study the expression and polymorphism of genes for cytokines such as IL-1β, IL-17 and IL-8 in Moroccan patients infected with H. pylori. ii) explore the activation of the NLRP3 inflammasome by H. pylori and determine the mechanisms involved in the activation of this complex by RNA viruses; known as defined activators of NLRP3.Our results underlined a high prevalence of H. pylori and demonstrated a cytokine signature: it can predict metaplasia during the progression of H. pylori infection involving a decrease in IL17A expression in the antrum and increased expression of IL-1β in the fundus. In particular, the genetic polymorphisms of IL-1β (IL-1β -31 and -511) do not appear to influence IL-1β expression significantly.In view of the difficulties encountered in isolating and culturing H. pylori, we used LPS from H. pylori to stimulate the inflammasome. Our results show that the transfection of cells in vitro with bacterial LPS induces the production of IL-1β which appears to be modulated by caspase 4, NOD1 and NOD2. Furthermore, while it is clearly established that RNA viruses induce activation of the NLRP3 inflammasome, the mechanisms by which these viruses induce IL-1β production are not well understood and remain to be confirmed. The results of this part of the work showed that the replication of cytopathogenic RNA viruses such as vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMCV) induces lytic cell death leading to an efflux of potassium which triggers activation of the NLRP3 inflammasome. Thus, viruses with a high replication capacity and which have a cytopathic effect are capable of inducing the activation of caspase-1 leading to the production of IL-1β. Conversely, viruses which induce type I IFN response are very poor inducers of the NLRP3 inflammasome.A better understanding of the activation of the inflammasome could help in the development of targeted therapeutic strategies for use in the fight against bacterial and viral infections.Key words: Helicobacter pylori, inflammation, NLRP3 inflammasome, IL-1β, RNA virus
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Books on the topic "INTERFERON SIGNATURE"

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Buckalew, Nelly A. Pain and Addiction in Older Adults (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0031.

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Addressing unique effects of both addiction and analgesia on older adults, this chapter defines the geriatric population and proceeds to discuss the recognition of addiction or substance misuse in it. There is little argument that the elderly have special diagnostic concerns and management needs that are imposed upon those of younger adults. The concept of the pain signature is introduced as a measure of the functions with which the individual’s pain interferes. Four instruments serving as diagnostic aids are included in tabular format: the pain signature elements; a list of recommended patient history queries; suggested components of the review of systems; and special components of the physical examination. The tables are geared specifically toward geriatric patients. The two central themes of the chapter are treatment of pain, and the treatment of opioid misuse and addiction.
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Book chapters on the topic "INTERFERON SIGNATURE"

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Osafo, Newman, and Silvio Owusu Dei. "Interferon Signature Analysis." In Reference Module in Biomedical Sciences. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-818731-9.00073-2.

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Aiman, Ayesha, Seemi Farhat Basir, and Asimul Islam. "Interferons Horizon Therapeutics." In Interferon - Immune Metabolism [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104718.

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Interferons (IFNs) are a family of multi-functional proteins, called cytokines, that are produced by immune cells such as leukocytes, natural killer (NK) cells, macrophages, fibroblasts, and epithelial cells. The minute amount of these α-helical glycoproteins, produced by mammalian cells, are firm components of the innate arm of the immune system providing rapid and broad protection against numerous types of invading pathogens. Interferons, from their discovery in the 19th century, have always held out a promise of important clinical utility first as an antiviral agent and more recently holding anti-inflammatory and regenerative effects for treating various neurological diseases such as multiple sclerosis, encephalopathies, Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), etc. IFNs elicit anti-viral and anti-inflammatory properties by inducing transcription of multiple IFN stimulated genes (ISG), a response that is partly mediated by Interferon regulatory factors (IRFs). This chapter provides a brief introduction of the interferon system as well as an in-depth assessment of the interferon signature and the various assay procedures for synthesizing non-natural interferon analogs for structural analysis, which may be helpful in designing improved products and act as a diagnostic tool for neurodegenerative disorders.
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Conference papers on the topic "INTERFERON SIGNATURE"

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Han, Shuhong, Haoyang Zhuang, Pui Lee, Mingjia Li, Peter Nigrovic, and Westley H. Reeves. "186 NRF2 regulation of the interferon signature in lupus macrophages." In 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.186.

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Mendoza, FA, S. Piera-Velazquez, P. Wermuth, S. Addya, C. Feghali-Bostwick, and SA Jimenez. "OP0096 Interferon signature in systemic sclerosis lung microvascular endothelial cells." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3739.

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Rönnblom, L. "SP0174 The value of type i interferon signature to stratify patients." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7782.

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Yun, J. H., S. Lee, R. Chase, M. M. Parker, A. Saferali, M. Seo, P. Castaldi, and C. P. Hersh. "Interferon-Inducible Blood Gene Expression Signature in COPD Patients with CT Airway Disease Phenotypes." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4052.

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Tesser, Alessandra, Gian Marco Moneta, Antonella Insalaco, Rebecca Nicolai, Claudia Bracaglia, Valentina Moressa, Serena Pastore, et al. "AB1062 INTER-LABORATORY COMPARISON OF TYPE I INTERFERON SIGNATURE ANALYSES: PAVING THE WAY TO SHARE RECOMMENDATIONS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7041.

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Yun, J. H., S. Lee, R. Chase, A. Saferali, J. Morrow, R. P. Bowler, P. Castaldi, and C. P. Hersh. "An Interferon Inducible Signature of Airway Disease from Gene Expression Profiling of Peripheral Blood from COPDGene." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4467.

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Lambers, W., J. Westra, B. Doornbos, MF Jonkman, H. Bootsma, and K. de Leeuw. "PS1:5 Interferon signature is increased in incomplete sle and correlates with mxa and ip-10 levels." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.54.

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Sikder, Rahmat K., Wafik S. El-Deiry, and Philip H. Abbosh. "Abstract 405: PBRM1 re-introduction inPBRM1-mutant kidney cancer cell lines drives an Interferon-γ expression signature." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-405.

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Hubbard, Erika, David S. Pisetsky, and Peter Lipsky. "1707 Anti-RNP antibodies are associated with the interferon gene signature but not complement activation in SLE." In LUPUS 21ST CENTURY 2021 CONFERENCE, Abstracts of the Fifth Biannual Scientific Meeting of the North and South American and Caribbean Lupus Community, Tucson, Arizona, USA – September 22–25, 2021. Lupus Foundation of America, 2021. http://dx.doi.org/10.1136/lupus-2021-lupus21century.102.

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Vlachogiannis, NI, V.-K. Bournia, A. Nezos, PF Christopoulos, M. Patsouras, PG Vlachoyiannopoulos, CP Mavragani, and PP Sfikakis. "THU0028 Type i interferon signature in the peripheral blood and CXCL4 plasma levels in patients with systemic sclerosis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4066.

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Reports on the topic "INTERFERON SIGNATURE"

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Shpigel, Nahum, Raul Barletta, Ilan Rosenshine, and Marcelo Chaffer. Identification and characterization of Mycobacterium paratuberculosis virulence genes expressed in vivo by negative selection. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7696510.bard.

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Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of a severe inflammatory bowel disease (IBD) in ruminants, known as Johne’s disease or paratuberculosis. Johne’s disease is considered to be one of the most serious diseases affecting dairy cattle both in Israel and worldwide. Heavy economic losses are incurred by dairy farmers due to the severe effect of subclinical infection on milk production, fertility, lower disease resistance and early culling. Its influence in the United States alone is staggering, causing an estimated loss of $1.5 billion to the agriculture industry every year. Isolation of MAP from intestinal tissue and blood of Crohn's patients has lead to concern that it plays a potential pathogenic role in promoting human IDB including Crohn’s disease. There is great concern following the identification of the organism in animal products and shedding of the organism to the environment by subclinically infected animals. Little is known about the molecular basis for MAP virulence. The goal of the original proposed research was to identify MAP genes that are required for the critical stage of initial infection and colonization of ruminants’ intestine by MAP. We proposed to develop and use signature tag mutagenesis (STM) screen to find MAP genes that are specifically required for survival in ruminants upon experimental infection. This research projected was approved as one-year feasibility study to prove the ability of the research team to establish the animal model for mutant screening and alternative in-vitro cell systems. In Israel, neonatal goat kids were repeatedly inoculated with either one of the following organisms; MAP K-10 strain and three transposon mutants of K-10 which were produced and screened by the US PI. Six months after the commencement of inoculation we have necropsied the goats and taken multiple tissue samples from the jejunum, ileum and mesenteric lymph nodes. Both PCR and histopathology analysis indicated on efficient MAP colonization of all the inoculated animals. We have established several systems in the Israeli PI’s laboratory; these include using IS900 PCR for the identification of MAP and using HSP65-based PCR for the differentiation between MAV and MAP. We used Southern blot analysis for the differentiation among transposon mutants of K-10. In addition the Israeli PI has set up a panel of in-vitro screening systems for MAP mutants. These include assays to test adhesion, phagocytosis and survival of MAP to/within macrophages, assays that determine the rate of MAPinduced apoptosis of macrophages and MAP-induced NO production by macrophages, and assays testing the interference with T cell ã Interferon production and T cell proliferation by MAP infected macrophages (macrophage studies were done in BoMac and RAW cell lines, mouse peritoneal macrophages and bovine peripheral blood monocytes derived macrophages, respectively). All partners involved in this project feel that we are currently on track with this novel, highly challenging and ambitious research project. We have managed to establish the above described research systems that will clearly enable us to achieve the original proposed scientific objectives. We have proven ourselves as excellent collaborative groups with very high levels of complementary expertise. The Israeli groups were very fortunate to work with the US group and in a very short time period to master numerous techniques in the field of Mycobacterium research. The Israeli group has proven its ability to run this complicated animal model. This research, if continued, may elucidate new and basic aspects related to the pathogenesis MAP. In addition the work may identify new targets for vaccine and drug development. Considering the possibility that MAP might be a cause of human Crohn’s disease, better understanding of virulence mechanisms of this organism might also be of public health interest as well.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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