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      The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism

      review-article
      Author(s): , *
      Publication date (Electronic):
      Journal: International Journal of Inflammation
      Publisher: Hindawi

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          Abstract

          Toll-like receptors (TLRs), part of the innate immune system that recognises molecular signatures, are important in the recognition of pathogenic components. However, when specific cellular contexts develop in which TLRs are inappropriately activated by self-components, this may lead to sterile inflammation and result in the occurrence of autoimmunity. This review analyses the available data regarding TLR biochemistry, the specific mechanisms which are brought about by TLR activation, and the importance of these mechanisms in the light of any existing and potential therapies in the field of autoimmunity.

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          Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA.

          Sandra S. Diebold, Tsuneyasu Kaisho, Hiroaki Hemmi … (2004)
          Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-alpha in response to the wild-type influenza virus. Here, we show that this requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production of inflammatory cytokines. These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.
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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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              Recognition of single-stranded RNA viruses by Toll-like receptor 7.

              Jennifer Lund, Lena Alexopoulou, Ayuko Sato … (2004)
              Viral infection of mammalian host results in the activation of innate immune responses. Toll-like receptors (TLRs) have been shown to mediate the recognition of many types of pathogens, including viruses. The genomes of viruses possess unique characteristics that are not found in mammalian genomes, such as high CpG content and double-stranded RNA. These genomic nucleic acids serve as molecular signatures associated with viral infections. Here we show that TLR7 recognizes the single-stranded RNA viruses, vesicular stomatitis virus and influenza virus. The recognition of these viruses by plasmacytoid dendritic cells and B cells through TLR7 results in their activation of costimulatory molecules and production of cytokines. Moreover, this recognition required intact endocytic pathways. Mice deficient in either the TLR7 or the TLR adaptor protein MyD88 demonstrated reduced responses to in vivo infection with vesicular stomatitis virus. These results demonstrate microbial ligand recognition by TLR7 and provide insights into the pathways used by the innate immune cells in the recognition of viral pathogens.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Inflam
                Journal ID (iso-abbrev): Int J Inflam
                Journal ID (publisher-id): IJI
                Title: International Journal of Inflammation
                Publisher: Hindawi
                ISSN (Print): 2090-8040
                ISSN (Electronic): 2042-0099
                Publication date (Print): 2017
                Publication date (Electronic): 3 May 2017
                Volume: 2017
                Electronic Location Identifier: 8391230
                Affiliations
                Centre for Molecular Medicine and Biobanking, Faculty of Medicine and Surgery, University of Malta, Msida MSD 2080, Malta
                Author notes

                Academic Editor: B. L. Slomiany

                Author information
                http://orcid.org/0000-0001-5722-6295
                Article
                DOI: 10.1155/2017/8391230
                PMC ID: 5434307
                PubMed ID: 28553556
                SO-VID: 7d5d270a-331e-461c-b1ca-705026b2a610
                Copyright © Copyright © 2017 Mark Farrugia and Byron Baron.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 10 January 2017
                Date revision received : 9 April 2017
                Date accepted : 11 April 2017
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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