For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
32
views
75
references
 Top references
cited by
80
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      859
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Roles of circular RNAs in immune regulation and autoimmune diseases

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Circular RNAs (circRNAs), as a novel class of endogenously expressed non-coding RNAs (ncRNAs), have a high stability and often present tissue-specific expression and evolutionary conservation. Emerging evidence has suggested that circRNAs play an essential role in complex human pathologies. Notably, circRNAs, important gene modulators in the immune system, are strongly associated with the occurrence and development of autoimmune diseases. Here, we focus on the roles of circRNAs in immune cells and immune regulation, highlighting their potential as biomarkers and biological functions in autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), primary biliary cholangitis (PBC), and psoriasis, aiming at providing new insights into the diagnosis and therapy of these diseases.

          Related collections

          Most cited references75

          • Record: found
          • Abstract: found
          • Article: not found

          Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations.

          Jlenia Guarnerio, Marco Bezzi, Jong Jeong … (2016)
          Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.
          Article 0 comments Cited 317 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Coordinated circRNA Biogenesis and Function with NF90/NF110 in Viral Infection

            Xiang Li, Chu-Xiao Liu, Wei Xue … (2017)
            Circular RNAs (circRNAs) generated via back-splicing are enhanced by flanking complementary sequences. Expression levels of circRNAs vary under different conditions, suggesting participation of protein factors in their biogenesis. Using genome-wide siRNA screening that targets all human unique genes and an efficient circRNA expression reporter, we identify double-stranded RNA-binding domain containing immune factors NF90/NF110 as key regulators in circRNA biogenesis. NF90/NF110 promote circRNA production in the nucleus by associating with intronic RNA pairs juxtaposing the circRNA-forming exon(s); they also interact with mature circRNAs in the cytoplasm. Upon viral infection, circRNA expression is decreased, in part owing to the nuclear export of NF90/NF110 to the cytoplasm. Meanwhile, NF90/NF110 released from circRNP complexes bind to viral mRNAs as part of their functions in antiviral immune response. Our results therefore implicate a coordinated regulation of circRNA biogenesis and function by NF90/NF110 in viral infection.
            Article 0 comments Cited 301 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Psoriasis.

              Jacqueline E Greb, Ari M Goldminz, James Elder … (2016)
              Psoriasis is a chronic, immune-mediated disorder with cutaneous and systemic manifestations and substantial negative effects on patient quality of life. Psoriasis has a strong, albeit polygenic, genetic basis. Whereas approximately half of the accountable genetic effect of psoriasis maps to the major histocompatibility complex, >70 other loci have been identified, many of which implicate nuclear factor-κB, interferon signalling and the IL-23-IL-23 receptor axis. Psoriasis pathophysiology is characterized by abnormal keratinocyte proliferation and immune cell infiltration in the dermis and epidermis involving the innate and adaptive immune systems, with important roles for dendritic cells and T cells, among other cells. Frequent comorbidities are rheumatological and cardiovascular in nature, in particular, psoriatic arthritis. Current treatments for psoriasis include topical agents, photo-based therapies, traditional systemic drugs and biologic agents. Treatments can be used in combination or as monotherapy. Biologic therapies that target specific disease mediators have become a mainstay in the treatment of moderate-to-severe disease, whereas advances in the treatment of mild-to-moderate disease have been limited.
              Article 0 comments Cited 299 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Lingling Zhao:
                ORCID: http://orcid.org/0000-0002-4118-1691
                +0371-66278520 , zhaolingling6@163.com
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 26 June 2019
                Publication date PMC-release: 26 June 2019
                Publication date Collection: July 2019
                Volume: 10
                Issue: 7
                Electronic Location Identifier: 503
                Affiliations
                [1 ]GRID grid.412633.1, Department of Chinese Medicine, , The First Affiliated Hospital of Zhengzhou University, ; Zhengzhou, 450000 China
                [2 ]ISNI 0000 0001 0379 7164, GRID grid.216417.7, Department of Clinical Pharmacology, Xiangya Hospital, , Central South University, ; Changsha, 410000 China
                [3 ]ISNI 0000 0001 0379 7164, GRID grid.216417.7, Hunan Key Laboratory of Pharmacogenetics, Institute of Clinical Pharmacology, , Central South University, ; Changsha, 410000 China
                Author information
                http://orcid.org/0000-0002-4118-1691
                Article
                Publisher ID: 1744
                DOI: 10.1038/s41419-019-1744-5
                PMC ID: 6594938
                PubMed ID: 31243263
                SO-VID: d529ab8c-e226-420a-809c-be0066b1ca2d
                Copyright © © The Author(s) 2019
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 5 May 2019
                Date revision received : 8 June 2019
                Date accepted : 12 June 2019
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Cell biology
                Keywords: immunopathogenesis,autoimmunity
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: immunopathogenesis, autoimmunity

                Comments

                Comment on this article

                scite_

                Similar content859

                See all similar

                Cited by85

                See all cited by