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      Interferon pathway in SLE: one key to unlocking the mystery of the disease

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          Abstract

          SLE is characterised by an activation of the interferon (IFN) system, which leads to an increased expression of IFN-regulated genes. The reasons behind the IFN signature in SLE are (1) the existence of endogenous IFN inducers, (2) activation of several IFN-producing cell types, (3) production of many different IFNs, (4) a genetic setup promoting IFN production and (5) deficient negative feedback mechanisms. The consequences for the immune system is a continuous stimulation to an immune response, and for the patient a number of different organ manifestations leading to typical symptoms for SLE. In the current review, we will present the existing knowledge of the IFN system and pathway activation in SLE. We will also discuss how this information can contribute to our understanding of both the aetiopathogenesis and some organ manifestations of the disease. We will put forward some issues that are unresolved and should be clarified in order to make a proper stratification of patients with SLE, which seems important when selecting a therapy aiming to downregulate the IFN system.

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          Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus.

          E. Baechler, F Batliwalla, G Karypis … (2003)
          Systemic lupus erythematosus (SLE) is a complex, inflammatory autoimmune disease that affects multiple organ systems. We used global gene expression profiling of peripheral blood mononuclear cells to identify distinct patterns of gene expression that distinguish most SLE patients from healthy controls. Strikingly, about half of the patients studied showed dysregulated expression of genes in the IFN pathway. Furthermore, this IFN gene expression "signature" served as a marker for more severe disease involving the kidneys, hematopoetic cells, and/or the central nervous system. These results provide insights into the genetic pathways underlying SLE, and identify a subgroup of patients who may benefit from therapies targeting the IFN pathway.
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            Interferon-Stimulated Genes: What Do They All Do?

            John W Schoggins (2019)
            In the absence of an intact interferon (IFN) response, mammals may be susceptible to lethal viral infection. IFNs are secreted cytokines that activate a signal transduction cascade leading to the induction of hundreds of interferon-stimulated genes (ISGs). Remarkably, approximately 10% of the genes in the human genome have the potential to be regulated by IFNs. What do all of these genes do? It is a complex question without a simple answer. From decades of research, we know that many of the protein products encoded by these ISGs work alone or in concert to achieve one or more cellular outcomes, including cell intrinsic antiviral defense, antiproliferative activities, and stimulation of adaptive immunity. The focus of this review is the antiviral activities of the IFN/ISG system. This includes general paradigms of ISG function, supported by specific examples in the literature, as well as methodologies to identify and characterize ISG function. Expected final online publication date for the Annual Review of Virology Volume 6 is September 30, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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              STAT4 and the risk of rheumatoid arthritis and systemic lupus erythematosus.

              Elaine Remmers, Robert Plenge, Annette T. Lee … (2007)
              Rheumatoid arthritis is a chronic inflammatory disease with a substantial genetic component. Susceptibility to disease has been linked with a region on chromosome 2q. We tested single-nucleotide polymorphisms (SNPs) in and around 13 candidate genes within the previously linked chromosome 2q region for association with rheumatoid arthritis. We then performed fine mapping of the STAT1-STAT4 region in a total of 1620 case patients with established rheumatoid arthritis and 2635 controls, all from North America. Implicated SNPs were further tested in an independent case-control series of 1529 patients with early rheumatoid arthritis and 881 controls, all from Sweden, and in a total of 1039 case patients and 1248 controls from three series of patients with systemic lupus erythematosus. A SNP haplotype in the third intron of STAT4 was associated with susceptibility to both rheumatoid arthritis and systemic lupus erythematosus. The minor alleles of the haplotype-defining SNPs were present in 27% of chromosomes of patients with established rheumatoid arthritis, as compared with 22% of those of controls (for the SNP rs7574865, P=2.81x10(-7); odds ratio for having the risk allele in chromosomes of patients vs. those of controls, 1.32). The association was replicated in Swedish patients with recent-onset rheumatoid arthritis (P=0.02) and matched controls. The haplotype marked by rs7574865 was strongly associated with lupus, being present on 31% of chromosomes of case patients and 22% of those of controls (P=1.87x10(-9); odds ratio for having the risk allele in chromosomes of patients vs. those of controls, 1.55). Homozygosity of the risk allele, as compared with absence of the allele, was associated with a more than doubled risk for lupus and a 60% increased risk for rheumatoid arthritis. A haplotype of STAT4 is associated with increased risk for both rheumatoid arthritis and systemic lupus erythematosus, suggesting a shared pathway for these illnesses. Copyright 2007 Massachusetts Medical Society.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Lupus Sci Med
                Journal ID (iso-abbrev): Lupus Sci Med
                Journal ID (hwp): lupusscimed
                Journal ID (publisher-id): lupus
                Title: Lupus Science & Medicine
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Electronic): 2053-8790
                Publication date Collection: 2019
                Publication date (Electronic): 13 August 2019
                Volume: 6
                Issue: 1
                Electronic Location Identifier: e000270
                Affiliations
                [1]departmentDepartment of Medical Sciences, Rheumatology , Uppsala University , Uppsala, Sweden
                Author notes
                [Correspondence to ] Professor Lars Rönnblom; lars.ronnblom@ 123456medsci.uu.se
                Author information
                http://orcid.org/0000-0001-9403-6503
                Article
                Publisher ID: lupus-2018-000270
                DOI: 10.1136/lupus-2018-000270
                PMC ID: 6703304
                PubMed ID: 31497305
                SO-VID: a4582051-676d-4c79-ab15-bc9f20d3eb72
                Copyright © © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
                License:

                This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See:  http://creativecommons.org/licenses/by-nc/4.0/.

                History
                Date received : 18 June 2019
                Date revision received : 19 July 2019
                Date accepted : 30 July 2019
                Funding
                Funded by: the Swedish Research Council;
                Funded by: Swedish Society of Medicine (the Ingegerd Johansson donation);
                Funded by: the Swedish Rheumatism Association;
                Funded by: King Gustaf V's 80-years Foundation;
                Categories
                Subject: Review
                Subject: 1506
                Custom metadata
                special-feature unlocked

                Keywords: systemic lupus erythematosus,interferon,plasmacytoid dendritic cell
                Data availability:
                Keywords: systemic lupus erythematosus, interferon, plasmacytoid dendritic cell

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