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Journal articles on the topic 'INTERFERON SIGNATURE'

Author: Grafiati

Published: 1 April 2023

Last updated: 26 July 2025

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1

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

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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 IFN

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2

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

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3

Smith, Michael Alexander, Chia-Chien Chiang, Dominic Sinibaldi, et al. "Using the Circulating Proteome to Assess Type I Interferon Activity in Systemic Lupus Erythematosus." Journal of Immunology 198, no. 1_Supplement (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, w

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4

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 (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 backgro

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Rigolet, Muriel, Cyrielle Hou, Yasmine Baba Amer, et al. "Distinct interferon signatures stratify inflammatory and dysimmune myopathies." RMD Open 5, no. 1 (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. Quantif

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6

Ramana, Chilakamarti V. "Regulation of a Metabolic Gene Signature in Response to Respiratory Viruses and Type I Interferon Signaling." Journal of Molecular Pathology 5, no. 1 (2024): 133–52. http://dx.doi.org/10.3390/jmp5010009.

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Respiratory viruses are the causative agents responsible for seasonal epidemics and occasional pandemic outbreaks and are a leading cause of death worldwide. Type I interferon (IFNα/β) signaling in the lung epithelial cells plays a major role in the innate immunity to respiratory viruses. Gene signatures are a set of differentially expressed genes in a particular disease or condition and are used to diagnose, monitor, and predict disease progression. These signatures can be used to identify regulatory modules and gene regulatory networks (GRNs) in mammalian signal transduction pathways. Consid

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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 constru

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Vavougios, George D., Theodoros Mavridis, Triantafyllos Doskas, Olga Papaggeli, Pelagia Foka, and Georgios Hadjigeorgiou. "SARS-CoV-2-Induced Type I Interferon Signaling Dysregulation in Olfactory Networks Implications for Alzheimer’s Disease." Current Issues in Molecular Biology 46, no. 5 (2024): 4565–79. http://dx.doi.org/10.3390/cimb46050277.

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Type I interferon signaling (IFN-I) perturbations are major drivers of COVID-19. Dysregulated IFN-I in the brain, however, has been linked to both reduced cognitive resilience and neurodegenerative diseases such as Alzheimer’s. Previous works from our group have proposed a model where peripheral induction of IFN-I may be relayed to the CNS, even in the absence of fulminant infection. The aim of our study was to identify significantly enriched IFN-I signatures and genes along the transolfactory route, utilizing published datasets of the nasal mucosa and olfactory bulb amygdala transcriptomes of

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9

Gallay, Laure, Guy Mouchiroud, and Bénédicte Chazaud. "Interferon-signature in idiopathic inflammatory myopathies." Current Opinion in Rheumatology 31, no. 6 (2019): 634–42. http://dx.doi.org/10.1097/bor.0000000000000653.

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10

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

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11

Tragin, Margot, Séverine A. Degrelle, Baptiste Periou, et al. "Muscle Spatial Transcriptomic Reveals Heterogeneous Profiles in Juvenile Dermatomyositis and Persistence of Abnormal Signature After Remission." Cells 14, no. 12 (2025): 939. https://doi.org/10.3390/cells14120939.

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This study aimed to investigate the spatial heterogeneity of molecular signature in the muscle of juvenile dermatomyositis (JDM) patients before and after treatment. Unsupervised reference-free deconvolution of spatial transcriptomics and standardized morphometry were performed in two JDM muscle biopsies with different clinical severity at disease onset and compared to healthy muscle. Identified signatures were scored in two additional JDM muscle biopsies from the same patient before and after remission. Disappearance of the normal muscle signature mostly corresponding to mitochondrial biology

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12

Magro, R., C. Saliba, L. Camilleri, C. Scerri, and A. Borg. "THU0235 VITAMIN D AND INTERFERON SIGNATURE GENE EXPRESSION IN SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 344.3–345. http://dx.doi.org/10.1136/annrheumdis-2020-eular.934.

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Background:Vitamin D deficiency is more prevalent in patients with systemic lupus eythematosus (SLE) as a result of sun avoidance.1The potential negative impact of vitamin D deficiency on SLE disease activity has been shown in a number of studies.2The expression of the interferon signature genes in SLE correlates positively with disease activity, and these genes are thought to mediate the clinical manifestations of the disease.3Objectives:The aim of this study was to establish whether a relationship exists between serum 25-hydroxyvitamin D level and the interferon signature gene expression in

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Li, Xuanyi, Ben Ho Park, Justin M. Balko та Douglas Buckner Johnson. "Pathway enrichment analysis in tumors with high mutation burdens and interferon-γ signature expression: A pancancer analysis." Journal of Clinical Oncology 41, № 16_suppl (2023): 3138. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.3138.

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3138 Background: Tumor mutation burden (TMB) correlates with immunotherapy response, but outcomes still vary in high TMB cancers, and many high TMB tumors lack T cell infiltration. Here, we assessed gene expression signatures of high TMB, including both inflamed and non-inflamed tumors (defined by interferon-γ [IFN-γ] gene signatures). Methods: Gene set enrichment analysis (GSEA) was assessed from RNA-sequencing data in tumors in TCGA. TMB and IFN-γ signature score were assessed by previously published methods. We performed GSEA on high vs low TMB tumors, and further stratified by high vs low

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Wu, Kang, Hai Fang, Liang-Dong Lyu, Douglas B. Lowrie, Ka-Wing Wong, and Xiao-Yong Fan. "A Derived Network-Based Interferon-Related Signature of Human Macrophages Responding toMycobacterium tuberculosis." BioMed Research International 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/713071.

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Network analysis of transcriptional signature typically relies on direct interaction between two highly expressed genes. However, this approach misses indirect and biological relevant interactions through a third factor (hub). Here we determine whether a hub-based network analysis can select an improved signature subset that correlates with a biological change in a stronger manner than the original signature. We have previously reported an interferon-related transcriptional signature (THP1r2Mtb-induced) fromMycobacterium tuberculosis(M. tb)-infected THP-1 human macrophage. We selected hub-conn

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Wigston, Z., A. Burska, A. Alase, K. Mahmoud, and E. Vital. "OP0091 A TWO-SCORE INTERFERON SIGNATURE AND MUSCULOSKELETAL IMAGING EXPLAIN THE ASSOCIATION BETWEEN INTERFERON AND ARTHRITIS IN SLE." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 60.2–60. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3564.

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Background:Interferon (IFN) signature is associated with disease activity and flare in SLE. We previously described two independent IFN gene expression scores; IFN Score A (the most commonly measured ISGs) and IFN Score B (less commonly measured ISGs which may also respond to IFN-II or other immune mediators)[1]. Many more clinical outcomes are associated with IFN Score B than with a “classic” interferon signature. These include progression of At-Risk individuals to SLE, response to rituximab, and differentiation of IFN signature in RA and SLE.In previous work, the relationship of IFN Signatur

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16

Templeton, Amanda K., N. Dominguez, R. Lu, et al. "IRF5 Genetic Risk Haplotype Influences Host B Cell Gene Responses to Epstein-Barr Virus (EBV) (49.14)." Journal of Immunology 182, no. 1_Supplement (2009): 49.14. http://dx.doi.org/10.4049/jimmunol.182.supp.49.14.

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Abstract Both gene and environment interactions play keyroles in the development of systemic lupus erythematosus (SLE). We examined effects of the IRF5 lupus risk haplotype upon the host's B cell response to the binding or infection with EBV, a suspected environmental trigger for SLE. Whole genome microarray expression profile data was collected from cells exposed to EBV for 16 hours. Analysis of gene expression by gene set enrichment analysis revealed that key differences in expression between SLE patients and controls (or individuals carrying the IRF5 risk and non-risk haplotype) were in a s

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17

Vieira, Matheus, Paul Régnier, Anna Maciejewski-Duval, et al. "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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18

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

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19

Sadanandam, Anguraj, Pawan Poudel, Elisa Fontana, and Chanthirika Ragulan. "Characterizing heterogeneity in KRAS mutant colorectal cancers (CRC) using cellular, mutation, and immune profiles." Journal of Clinical Oncology 36, no. 4_suppl (2018): 657. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.657.

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657 Background: Approximately 30%-50% of CRC patients have KRAS mutation, and they are associated with lack of treatment response to anti-EGFR therapy. KRAS mutant CRCs are heterogeneous that not all mutant tumors are dependent on its downstream signaling. At this era of the search for therapeutic targets related to mutant KRAS, it is essential to understand the underlying heterogeneity in KRAS mutant metastatic CRCs with a goal of identifying personalized therapeutic vulnerabilities. To understand KRAS mutation further, in this study we classified KRAS mutant CRCs based on individual cell typ

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20

Guthridge, Joel M., Daniel N. Clark, Amanda Templeton, et al. "Effects of IRF5 Lupus Risk Haplotype on Pathways Predicted to Influence B Cell Functions." Journal of Biomedicine and Biotechnology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/594056.

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Both genetic and environmental interactions affect systemic lupus erythematosus (SLE) development and pathogenesis. One known genetic factor associated with lupus is a haplotype of the interferon regulatory factor 5 (IRF5) gene. Analysis of global gene expression microarray data using gene set enrichment analysis identified multiple interferon- and inflammation-related gene sets significantly overrepresented in cells with the risk haplotype. Pathway analysis using expressed genes from the significant gene sets impacted by theIRF5risk haplotype confirmed significant correlation with the interfe

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21

Wu, Kang, Ka-Wing Wong, Wang-Long Deng, et al. "The Numerical Predominance and Large Transcriptome Differences of Neutrophils in Peripheral Blood Together Inevitably Account for a Reported Pulmonary Tuberculosis Signature." International Journal of Genomics 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/5830971.

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Previous transcriptomic analysis revealed a 393-transcript signature (PTBsig), which is dominated by interferon inducible genes, in whole blood of pulmonary tuberculosis (PTB) patients. Comparisons with a limited set of interferon-driven genes among separated monocytes, CD4+ T cells, CD8+ T cells, and neutrophils indicated that the signature is due to changes in neutrophils, the overwhelmingly predominant cell type. By extending the analysis to the entire 393 transcripts of PTBsig and by switching the cell proportions between separated monocytes, CD4+ T cells, CD8+ T cells, and neutrophils, we

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Gallucci, Stefania, Heather Bennett, Debra Shivers, et al. "Intrinsic Interferon Signature in Dendritic Cells in lupus-prone mice. (83.9)." Journal of Immunology 184, no. 1_Supplement (2010): 83.9. http://dx.doi.org/10.4049/jimmunol.184.supp.83.9.

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Abstract Type I Interferons (IFNs) are pathogenic in Systemic Lupus Erythematosus. PBMCs from lupus patients over-express Type I IFN responsive genes. The cause and cellular source of this "Interferon Signature" are still unclear. Since we found that dendritic cells (DCs) from lupus-prone mice express the IFN Signature, we asked whether this IFN Signature was intrinsic to the DCs. We found that bone marrow-derived dendritic cells (BMDCs) from young pre-diseased Sle1,2,3 lupus-prone mice constitutively over-express Type I IFN responsive genes, analyzed by real-time RT-PCR (IFN-a, IFN-b, STAT1,

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23

Wigston, Z., A. Burska, M. Wittmann, and E. Vital. "POS0179 EXPLORING THE EFFECTS OF A TWO-SCORE INTERFERON SIGNATURE AND RESPONSES TO INTERFERON STIMULUS." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 302.1–303. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1100.

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Background:IFN Scores are increasingly important as biomarkers to stratify RMDs and select patients for interferon targeted therapies. Several studies have previously demonstrated that different sets of interferon stimulated genes (ISGs) have different clinical associations. We validated a 2-score system of ISGs expression consisting of Score A (a set of ISGs included in most interferon signature assays) and Score B (a set of less commonly measured ISGs). Score B consistently demonstrated stronger clinical associations in studies of diagnosis, prediction of progression to SLE in At-Risk indivi

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Wu, Yu, Zhichao Wang, Houjia Hu, et al. "Identification of Immune-Related Gene Signature in Schizophrenia." Actas Españolas de Psiquiatría 52, no. 3 (2024): 276–88. http://dx.doi.org/10.62641/aep.v52i3.1648.

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Background: Schizophrenia (SCZ) is a type of psychiatric disorder characterized by multiple symptoms. Our aim is to decipher the relevant mechanisms of immune-related gene signatures in SCZ. Methods: The SCZ dataset and its associated immunoregulatory genes were retrieved using Gene Expression Omnibus (GEO) and single-sample gene set enrichment analysis (ssGSEA). Co-expressed gene modules were determined through weighted gene correlation network analysis (WGCNA). To elucidate the functional characteristics of these clusters, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG)

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Ahmed, Md Shakir Uddin, Tiffany Dorsey, and Stefan Ambs. "Abstract 6159: Single cell analysis of circulating peripheral blood mononuclear cells in African American men with prostate cancer and their association with lethal disease." Cancer Research 84, no. 6_Supplement (2024): 6159. http://dx.doi.org/10.1158/1538-7445.am2024-6159.

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Abstract Prostate cancer is a leading cause of cancer-related deaths among men in the United States and affects African American (AA) men more so than other men. We and others previously described a distinct tumor immunobiology in AA prostate cancer patients. Furthermore, we discovered a serum proteome-defined suppression of tumor immunity signature that is prevalent among these patients and associated with lethal prostate cancer. In the current study, we sought to investigate the composition of circulating peripheral blood mononuclear cells (PBMCs) in AA and European American (EA) prostate ca

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Komura, Kazuhiro, Yuki Ichimura, Naoko Okiyama, Kazuyoshi Watanabe, Hiroaki Muramoto, and Takashi Matsushita. "Interferon signature in cutaneous lesion of COVID toes." Journal of Immunology 206, no. 1_Supplement (2021): 20.37. http://dx.doi.org/10.4049/jimmunol.206.supp.20.37.

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Abstract Increasing reports have showed several kinds of dermatological manifestation in Coronavirus disease 2019 (COVID-19). Some of them may occur as a direct implication of coronavirus infection. Within those, acral skin changes, recently called COVID toes, have a potential to provide a diagnostic value. We herein described a 49-year old Japanese man with COVID toes. The skin lesions appeared simultaneously with fever. The rash was similar for cold-induced erythema multiforme of the patients with familial Chilblain; hereditary type I interferonopathy. Histopathological staining indicated up

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Genova, Elena, Maura Apollonio, Giuliana Decorti, Alessandra Tesser, Alberto Tommasini, and Gabriele Stocco. "In Vitro Effects of Sulforaphane on Interferon-Driven Inflammation and Exploratory Evaluation in Two Healthy Volunteers." Molecules 26, no. 12 (2021): 3602. http://dx.doi.org/10.3390/molecules26123602.

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Interferonopathies are rare genetic conditions defined by systemic inflammatory episodes caused by innate immune system activation in the absence of pathogens. Currently, no targeted drugs are authorized for clinical use in these diseases. In this work, we studied the contribution of sulforaphane (SFN), a cruciferous-derived bioactive molecule, in the modulation of interferon-driven inflammation in an immortalized human hepatocytes (IHH) line and in two healthy volunteers, focusing on STING, a key-component player in interferon pathway, interferon signature modulation, and GSTM1 expression and

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Edgar, Contessa, Deirdra Terrell, Sara Vesely, et al. "Immune and ribosomal gene expression associate with relapse in ADAMTS13-deficient thrombotic thrombocytopenic purpura (P4086)." Journal of Immunology 190, no. 1_Supplement (2013): 51.9. http://dx.doi.org/10.4049/jimmunol.190.supp.51.9.

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Abstract 40% of patients who survive acute episodes of thrombotic thrombocytopenic purpura (TTP) associated with severe ADAMTS13 deficiency will relapse. Risk factors for relapse other than severe ADAMTS13 deficiency are unknown. ADAMTS13 autoantibodies, TTP episodes following infection or type I interferon treatment and reported ensuing systemic lupus erythematosus in some patients suggest immune dysregulation. This study asked whether ADAMTS13-deficient TTP patients in remission have peripheral blood transcriptional markers that associate with relapse history. Peripheral blood from 38 patien

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Obermoser, G., та V. Pascual. "The interferon-α signature of systemic lupus erythematosus". Lupus 19, № 9 (2010): 1012–19. http://dx.doi.org/10.1177/0961203310371161.

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Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease’s unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and productio

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Farias Amorim, Camila, Fernanda O. Novais, Ba T. Nguyen та ін. "Localized skin inflammation during cutaneous leishmaniasis drives a chronic, systemic IFN-γ signature". PLOS Neglected Tropical Diseases 15, № 4 (2021): e0009321. http://dx.doi.org/10.1371/journal.pntd.0009321.

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Cutaneous leishmaniasis is a localized infection controlled by CD4+ T cells that produce IFN-γ within lesions. Phagocytic cells recruited to lesions, such as monocytes, are then exposed to IFN-γ which triggers their ability to kill the intracellular parasites. Consistent with this, transcriptional analysis of patient lesions identified an interferon stimulated gene (ISG) signature. To determine whether localized L. braziliensis infection triggers a systemic immune response that may influence the disease, we performed RNA sequencing (RNA-seq) on the blood of L. braziliensis-infected patients an

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Kuo, Hung-Yang, Jhe-Cyuan Guo, Chia-Lang Hsu, Ta-Chen Huang, and Chih-Hung Hsu. "The immunogenomic difference between Asian and non-Asian esophageal squamous cell carcinoma (ESCC) patients: An analysis of the Cancer Genome Atlas (TCGA) cohort." Journal of Clinical Oncology 38, no. 5_suppl (2020): 27. http://dx.doi.org/10.1200/jco.2020.38.5_suppl.27.

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27 Background: Recently reported global phase 3 trials of immune checkpoint inhibitor (ICI) versus second-line chemotherapy for esophageal cancer revealed that Asian population appear to obtain more benefit from ICI than non-Asian patients even in ESCC subgroups. Whether this observation could be explained by the immunogenomic difference between Asian and non-Asian ESCC remains uncertain. Methods: We retrieved the data of genetic alterations and gene expression profiling from ESCC patients of TCGA dataset, and compared the mutational profiles, immune subtypes, composition of immune cell infilt

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Radke, Josefine, Randi Koll, Corinna Preuße, et al. "Architectural B-cell organization in skeletal muscle identifies subtypes of dermatomyositis." Neurology - Neuroimmunology Neuroinflammation 5, no. 3 (2018): e451. http://dx.doi.org/10.1212/nxi.0000000000000451.

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ObjectiveTo study the B-cell content, organization, and existence of distinct B-cell subpopulations in relation to the expression of type 1 interferon signature related genes in dermatomyositis (DM).MethodsEvaluation of skeletal muscle biopsies from patients with adult DM (aDM) and juvenile DM (jDM) by histology, immunohistochemistry, electron microscopy, and quantitative reverse-transcription PCR.ResultsWe defined 3 aDM subgroups—classic (containing occasional B cells without clusters), B-cell–rich, and follicle-like aDM—further elucidating IM B-lymphocyte maturation and immunity. The quantit

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Raupov, R., E. Suspitsin, R. Mulkidzhan, and M. Kostik. "POS1312 ANALYSIS OF INTERFERON TYPE I SIGNATURE IN JUVENILE DERMATOMYOSITIS." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 993.3–994. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3292.

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Backgroundthe crucial role of hyperactivation IFN I signaling pathway has been proved in the pathogenesis of dermatomyositis. IFN I genes and chemokines activity vary according to subtype of inflammatory myopathies. IFN type 1 signature could be measured using different genes in the blood, skin and muscle tissue [1].Objectivesto evaluate IFN-score in children with dermatomyositis and compare with disease activityMethods15 patients (5 boys and 10 girls) were enrolled in the study. Clinical and laboratory parameters, disease activity (CMAS-childhood myositis assessment tool, aCAT- abbreviated cu

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Heimes, Anne-Sophie, Franziska Härtner, Katrin Almstedt та ін. "Prognostic Significance of Interferon-γ and Its Signaling Pathway in Early Breast Cancer Depends on the Molecular Subtypes". International Journal of Molecular Sciences 21, № 19 (2020): 7178. http://dx.doi.org/10.3390/ijms21197178.

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Interferons are crucial for adaptive immunity and play an important role in the immune landscape of breast cancer. Using microarray-based gene expression analysis, we examined the subtype-specific prognostic significance of interferon-γ (IFN-γ) as a single gene as well as an IFN-γ signature covering the signaling pathway in 461 breast cancer patients. Prognostic significance of IFN-γ, as well as the IFN-γ signature for metastasis-free survival (MFS), were examined using Kaplan–Meier as well as univariate and multivariate Cox regression analyses in the whole cohort and in different molecular su

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Raupov, R., E. Suspitsin, E. Kalashnikova, et al. "POS0078 CROSS-SECTIONAL ANALYSIS OF INTERFERON SIGNATURE IN PEDIATRIC SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 246.1–247. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1956.

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Background:the role of interferon pathways in the pathogenesis of systemic lupus erythematosus (SLE) has been proven over the past years. Existing data suggest that interferon score (IFN I score) may serve as a useful marker of disease activity and patient clinical characteristics.Objectives:to compare characteristics of pediatric SLE patients with high and normal IFN I score.Methods:40 SLE patients (33 girls, 7 boys) under 18 years old were included in the cross-sectional study. In all cases the diagnosis was made using Systemic Lupus International Collaborating Clinics (SLICC) classification

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Kostik, M., R. Raupov, R. Mulkidzhan, A. Kosmin, and E. Suspitsin. "AB0001 INTERFERON SIGNATURE IN CHILDREN WITH CHRONIC NON-BACTERIAL OSTEOMYELITIS AND IT’S DYNAMIC AFTER BISPHOSPHONATES TREATMENT." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 1036.2–1036. http://dx.doi.org/10.1136/annrheumdis-2021-eular.508.

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Background:Chronic non-bacterial osteomyelitis (CNO) is an immune-mediated chronic inflammatory bone disease which predominantly affects children and adolescents. The pathogenesis of CNO related to imbalance between pro-inflammatory and anti-inflammatory cytokines. Interferon-I mediated pathway is associated with pathogenesis of different pediatric rheumatic diseases, such as juvenile systemic lupus erythematosus (jSLE), juvenile dermatomyositis (JDM), systemic onset of juvenile idiopathic arthritis (soJIA), and, most of all, with macrophage activation syndrome. The data on interferon-I- regul

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Kossenkov, Andrew V., Andrew Milcarek, Faiyaz Notta, et al. "Mitochondrial fitness and cancer risk." PLOS ONE 17, no. 10 (2022): e0273520. http://dx.doi.org/10.1371/journal.pone.0273520.

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Changes in metabolism are a hallmark of cancer, but molecular signatures of altered bioenergetics to aid in clinical decision-making do not currently exist. We recently identified a group of human tumors with constitutively reduced expression of the mitochondrial structural protein, Mic60, also called mitofilin or inner membrane mitochondrial protein (IMMT). These Mic60-low tumors exhibit severe loss of mitochondrial fitness, paradoxically accompanied by increased metastatic propensity and upregulation of a unique transcriptome of Interferon (IFN) signaling and Senescence-Associated Secretory

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Shamitova, E. N., M. A. Dubinkina, and E. R. Khamidullova. "INTERFERON I SIGNATURE FOR DIFFERENTIAL DIAGNOSIS OF DISEASESOFTHE IMMUNESYSTEM." Научное обозрение. Биологические науки (Scientific Review. Biological Sciences), no. 2 2022 (2022): 48–53. http://dx.doi.org/10.17513/srbs.1272.

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Haupl, T., R. Biesen, B. Smiljanovic, et al. "The type 1 interferon signature: facts, fads and fallacies." Annals of the Rheumatic Diseases 70, Suppl 2 (2011): A24. http://dx.doi.org/10.1136/ard.2010.148965.26.

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Kondrateva, Liubov, Tatiana Panafidina, Yulia Gorbunova, Elena Tchetina, Anastasia Avdeeva, and Tatiana Popkova. "TYPE I INTERFERON GENES SIGNATURE AND GALECTINS-1,3,9: ARE THERE A RELATIONSHIPS?" Journal of Rheumatology 52, Suppl 1 (2025): 97.1–97. https://doi.org/10.3899/jrheum.2025-0390.pv032.

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PV032 / #459Poster Topic:AS04 - BiomarkersBackground/PurposeTo find out whether galectins-1,3,9 levels are related to the type I interferon genes signature (IFNGS) in patients with systemic lupus erythematosus (SLE).MethodsA total of 43 patients (38 women and 5 men) with SLE (31[23-41] years old) were enrolled in the study. The median SLE duration was 24 [1-96] months, SLEDAI-2K was 8 [4-14]. SLE pts were treated with glucocorticoids (GC) (72,12%), hydroxychloroquine (69,8%), immunosuppressive drugs (35,9%) and biological agents (4,7%). Type I interferon status was assessed as «low» or «high»

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

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

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Gallucci, Stefania, Linda Varghese, Heather Bennett, et al. "Intrinsic interferon signature in myeloid dendritic cells from lupus-prone mice precedes disease onset (47.1)." Journal of Immunology 186, no. 1_Supplement (2011): 47.1. http://dx.doi.org/10.4049/jimmunol.186.supp.47.1.

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Abstract Systemic Lupus Erythematosus (SLE) patients over-express Type I Interferon (IFN) responsive genes but the cellular source of this IFN Signature is unclear. We found that ex vivo dendritic cells (DCs) from Sle1,2,3 lupus-prone mice express the IFN Signature. To test if the IFN Signature was intrinsic to DCs, we grew myeloid DCs in vitro from bone marrow in GM-CSF medium (BMDCs), and found that IFN responsive genes, analyzed by real-time RT-PCR, are constitutively over-expressed in Sle1,2,3 BMDCs as compared to non-autoimmune C57BL/6 BMDCs: expression of IFN-b, signaling molecules IRF-7

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Khan, Sabbir, Rajasekaran Mahalingam, Shayak Sen, et al. "STEM-24. INTERFERON SIGNALING REGULATES THE PROLIFERATION AND MESENCHYMAL PHENOTYPE OF GLIOBLASTOMA STEM CELLS." Neuro-Oncology 23, Supplement_6 (2021): vi26. http://dx.doi.org/10.1093/neuonc/noab196.098.

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Abstract Interferon (IFN) signaling contributes to stemness, cell proliferation, cell death, and cytokine signaling in cancer and immune cells; however, the role of IFN signaling in glioblastoma (GBM) and GBM stem-like cells (GSCs) is unclear. This study aimed to investigate the cancer cell-intrinsic IFN signaling in tumorigenesis and malignant phenotype of GBM. We characterized cell-intrinsic IFN signaling in The Cancer Genome Atlas, patient-derived cohorts of GSCs, and published single-cell RNA sequencing datasets by in-silico analyses. The in-silico findings were further validated by evalua

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Skougaard, Marie, Sisse Bolm Ditlev, Magnus Friis Søndergaard та Lars Erik Kristensen. "Cytokine Signatures in Psoriatic Arthritis Patients Indicate Different Phenotypic Traits Comparing Responders and Non-Responders of IL-17A and TNFα Inhibitors". International Journal of Molecular Sciences 24, № 7 (2023): 6343. http://dx.doi.org/10.3390/ijms24076343.

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This study aimed to explore the dynamic interactions between 32 cytokines and biomarkers in Psoriatic Arthritis (PsA) patients to compare cytokine signatures of treatment responders and non-responders. Biomarkers were measured before and after four months of treatment in 39 PsA patients initiating either Tumor Necrosis Factor alpha inhibitor (TNFi) or Interleukin-17A inhibitor (IL-17Ai). Response to treatment was defined by the composite measure, Disease Activity in Psoriatic Arthritis (DAPSA). A two-component principal component analysis (PCA) was implemented to describe cytokine signatures c

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Garantziotis, Panagiotis, Georgia Savina Moysidou, Noemin Kapsala, et al. "Transcriptome analysis to decipher the molecular underpinnings of response to treatment in systemic lupus erythematosus." RMD Open 11, no. 1 (2025): e005050. https://doi.org/10.1136/rmdopen-2024-005050.

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ObjectiveSystemic lupus erythematosus (SLE) is a multisystem autoimmune disease characterised by variable treatment responses. We investigated the transcriptional landscape associated with treatment response and resistance in SLE.MethodsBlood was collected from 92 active patients with SLE at baseline and after 6 months (n=32 paired samples) of treatment with cyclophosphamide (n=40), rituximab (n=20), belimumab (n=23), mycophenolate mofetil (n=8) or azathioprine (n=1) and was subjected to RNA sequencing. The response was defined by the Lupus Low Disease Activity State. We identified differentia

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Costa, Raphael, Werbson Guaraná, Braziliano Júnior, et al. "OPHTHALMIC INVOLVEMENT IN SYSTEMIC LUPUS ERYTHEMATOSUS IS ASSOCIATED WITH INTERFERON-ALPHA GENE SIGNATURE: A CROSS-SECTIONAL STUDY." Journal of Rheumatology 52, Suppl 1 (2025): 138.2–138. https://doi.org/10.3899/jrheum.2025-0390.pv102.

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PV102 / #625Poster Topic:AS12 - Genetics, Epigenetics, TranscriptomicsBackground/PurposeInterferon Pathways studies have highlighted the role of type I interferons, especially interferon-alpha (IFN-α), in driving inflammatory pathways in lupus. Elevated levels of IFN-α are often associated with disease activity. However, few studies have been performed to clarify the role of IFN-α in ocular involvement, including dry eye and retinal changes in Systemic Erythematosus Lupus (SLE). We aimed to assess the association between IFN-α genes signature and ophthalmological involvement in SLE patients.Me

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Avdeeva, A. S., E. V. Tchetina, M. V. Cherkasova, et al. "The expression of interferon-stimulated genes (interferon “signature”) in patients with rheumatoid arthritis (Preliminary results)." Rheumatology Science and Practice 58, no. 6 (2021): 673–77. http://dx.doi.org/10.47360/1995-4484-2020-673-677.

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Buie, Joy, and James Oates. "Interferon alpha deregulates endothelial nitric oxide synthase (P4085)." Journal of Immunology 190, no. 1_Supplement (2013): 127.14. http://dx.doi.org/10.4049/jimmunol.190.supp.127.14.

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Abstract Background: Recent in vitro studies suggest that Type I interferons promote endothelial progenitor cell dysfunction and apoptosis while others have shown that Type I interferon gene signature correlates with increased endothelial dysfunction in systemic lupus erythematosus patients. Although causes of ED are likely multifactorial, all pathways converge on the diminished activity of endothelial nitric oxide synthase. We examined the effects of IFN-alpha on eNOS gene expression, phosphorylation, and NO production. Methods: Changes in eNOS expression in response to IFN-a (100, 1000 IU) w

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Gillezeau, Christina, Naimisha Movva, Maaike van Gerwen, et al. "Interferon gamma expression and mortality in unselected cohorts of urothelial bladder cancer patients." PLOS ONE 17, no. 8 (2022): e0271339. http://dx.doi.org/10.1371/journal.pone.0271339.

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Background The role of interferon gamma (IFN-γ) expression in long-term survival has not been studied in patients with urinary bladder cancer (UBC). IFN-γ expression was characterized among various UBC patient cohorts to assess if IFN-γ status is associated with overall survival (OS). Methods A tumor-based IFN-γ gene signature was evaluated among adult UBC patients newly diagnosed between 2004 and 2017 from two hospital systems in New York. Patient cohorts included metastatic (stage IV or progressing to stage IV [MBC]), muscle-invasive (stages T2a to T4a [MIBC]), and non–muscle-invasive (carci

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Haberman Ziv, Y., N. Loberman-Nachum, S. Katya, et al. "OP06 Comparison between Crohn and coeliac diseases small intestine transcriptomics and microbial data define similarities and divergent pathways linked to pathogenesis." Journal of Crohn's and Colitis 14, Supplement_1 (2020): S006. http://dx.doi.org/10.1093/ecco-jcc/jjz203.005.

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Abstract Background Crohn disease and coeliac disease are two inflammatory conditions known to cause small intestine inflammation. Using high throughput transcriptomics, microbial, and bioinformatics approaches we aimed to capture differences and similarities linked to the pathogenesis and to future potential interventions for those chronic manifestations. Methods We performed high throughput transcriptomics and 16S microbial characterisation of 55 paediatric new-onset coeliac patients and controls using clinical pathology specimens, and compared those signatures to our previously reported 248

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