For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
15
views
62
references
 Top references
cited by
22
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      342
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction

      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

          Atherosclerosis is characterized by early endothelial dysfunction and altered vascular smooth muscle cells (VSMCs) contractility. The forming atheroma is a site of excessive production of cytokines and inflammatory ligands by various cell types that mediate inflammation and immune responses. Key factors contributing to early stages of plaque development are IFNγ and TLR4. This review provides insight in the differential STAT1-dependent signal integration between IFNγ and TLR4 signals in vascular cells and atheroma interacting immune cells. This results in increased leukocyte attraction and adhesion and VSMC proliferation and migration, which are important characteristics of EC dysfunction and early triggers of atherosclerosis.

          Related collections

          Most cited references62

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

          The dorsoventral regulatory gene cassette spätzle/Toll/cactus controls the potent antifungal response in Drosophila adults.

          B. Lemaitre, E. Nicolás, L Michaut … (1996)
          The cytokine-induced activation cascade of NF-kappaB in mammals and the activation of the morphogen dorsal in Drosophila embryos show striking structural and functional similarities (Toll/IL-1, Cactus/I-kappaB, and dorsal/NF-kappaB). Here we demonstrate that these parallels extend to the immune response of Drosophila. In particular, the intracellular components of the dorsoventral signaling pathway (except for dorsal) and the extracellular Toll ligand, spätzle, control expression of the antifungal peptide gene drosomycin in adults. We also show that mutations in the Toll signaling pathway dramatically reduce survival after fungal infection. Antibacterial genes are induced either by a distinct pathway involving the immune deficiency gene (imd) or by combined activation of both imd and dorsoventral pathways.
          Article 0 comments Cited 369 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The IRF family transcription factors in immunity and oncogenesis.

            Tomohiko Tamura, Hideyuki Yanai, David Savitsky … (2008)
            The interferon regulatory factor (IRF) family, consisting of nine members in mammals, was identified in the late 1980s in the context of research into the type I interferon system. Subsequent studies over the past two decades have revealed the versatile and critical functions performed by this transcription factor family. Indeed, many IRF members play central roles in the cellular differentiation of hematopoietic cells and in the regulation of gene expression in response to pathogen-derived danger signals. In particular, the advances made in understanding the immunobiology of Toll-like and other pattern-recognition receptors have recently generated new momentum for the study of IRFs. Moreover, the role of several IRF family members in the regulation of the cell cycle and apoptosis has important implications for understanding susceptibility to and progression of several cancers.
            Article 0 comments Cited 350 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Spatiotemporal regulation of MyD88-IRF-7 signalling for robust type-I interferon induction.

              Kenya Honda, Yusuke Ohba, Hideyuki Yanai … (2005)
              Robust type-I interferon (IFN-alpha/beta) induction in plasmacytoid dendritic cells, through the activation of Toll-like receptor 9 (TLR9), constitutes a critical aspect of immunity. It is absolutely dependent on the transcription factor IRF-7, which interacts with and is activated by the adaptor MyD88. How plasmacytoid dendritic cells, but not other cell types (such as conventional dendritic cells), are able to activate the MyD88-IRF-7-dependent IFN induction pathway remains unknown. Here we show that the spatiotemporal regulation of MyD88-IRF-7 signalling is critical for a high-level IFN induction in response to TLR9 activation. The IFN-inducing TLR9 ligand, A/D-type CpG oligodeoxynucleotide (CpG-A), is retained for long periods in the endosomal vesicles of plasmacytoid dendritic cells, together with the MyD88-IRF-7 complex. However, in conventional dendritic cells, CpG-A is rapidly transferred to lysosomal vesicles. We further show that conventional dendritic cells can also mount a robust IFN induction if CpG-A is manipulated for endosomal retention using a cationic lipid. This strategy also allows us to demonstrate endosomal activation of the IFN pathway by the otherwise inactive TLR9 ligand B/K-type oligodeoxynucleotide (CpG-B). Thus, our study offers insights into the regulation of TLR9 signalling in space, potentially suggesting a new avenue for therapeutic intervention.
              Article 0 comments Cited 215 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): JAKSTAT
                Journal ID (iso-abbrev): JAKSTAT
                Journal ID (publisher-id): JKST
                Title: JAK-STAT
                Publisher: Landes Bioscience
                ISSN (Print): 2162-3988
                ISSN (Electronic): 2162-3996
                Publication date (Print): 01 October 2012
                Publication date (Electronic): 01 October 2012
                Publication date PMC-release: 01 October 2012
                Volume: 1
                Issue: 4
                Pages: 241-249
                Affiliations
                [1 ]Department of Human Molecular Genetics; Institute of Molecular Biology and Biotechnology; Faculty of Biology; Adam Mickiewicz University; Poznan, Poland
                [2 ]Department of Nephrology; Klinikum rechts der Isar; Technische Universität München; Munich, Germany
                Author notes
                [* ]Correspondence to: Hans Bluyssen, Email: h.bluyss@ 123456amu.edu.pl
                Article
                Publisher ID: 2012JAKS0052R Publisher Item ID: 22469
                DOI: 10.4161/jkst.22469
                PMC ID: 3670280
                PubMed ID: 24058779
                SO-VID: 15be45ae-32a4-4eff-b89b-0167115cf960
                Copyright © Copyright © 2012 Landes Bioscience
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                Categories
                Subject: Review

                Keywords: atherosclerosis,ifn-gamma,toll-like receptors,stat1,irfs,signal integration
                Data availability:
                Keywords: atherosclerosis, ifn-gamma, toll-like receptors, stat1, irfs, signal integration

                Comments

                Comment on this article

                scite_

                Similar content342

                See all similar

                Cited by20

                See all cited by

                Most referenced authors2,068

                See all reference authors