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      STAT2 : A shape-shifting anti-viral super STAT

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          Abstract

          STAT2 is unique among the STAT family of transcription factors in that its activation is driven predominantly by only two classes of cell surface receptors: Type I and III interferon receptors. As such, STAT2 plays a critical role in host defenses against viral infections. Viruses have evolved to target STAT2 by either inhibiting its expression, blocking its activity, or by targeting it for degradation. Consequently, these viral onslaughts have driven remarkable divergence in the STAT2 gene across species that is not observed in other STAT family members. Thus, the evolution of STAT2 may preserve its activity and protect each species in the face of an ever-changing viral community.

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          Plasmacytoid dendritic cells in immunity.

          Marco Colonna, Giorgio Trinchieri, Yong-Jun Liu (2004)
          Human and mouse plasmacytoid dendritic cells have been shown to correspond to a specialized cell population that produces large amounts of type I interferons in response to viruses, the so-called natural interferon-producing cells. As a result, intensive investigation is now focused on the potential functions of plasmacytoid dendritic cells in both innate and adaptive immunity. Here we review recent progress on the characterization of plasmacytoid dendritic cell origin, development, migration and function in immunity and tolerance, as well as their effect on human diseases.
          Article 0 comments Cited 360 times – based on 0 reviews     Review now
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            Novel role of PKR in inflammasome activation and HMGB1 release

            Ben Lu, Takahisa Nakamura, Karen Inouye … (2012)
            The inflammasome regulates release of caspase activation-dependent cytokines, including IL-1β, IL-18, and high-mobility group box 1 (HMGB1) 1-5 . During the course of studying HMGB1 release mechanisms, we discovered an important role of double-stranded RNA dependent protein kinase (PKR) in inflammasome activation. Exposure of macrophages to inflammasome agonists induced PKR autophosphorylation. PKR inactivation by genetic deletion or pharmacological inhibition severely impaired inflammasome activation in response to double-stranded RNA, ATP, monosodium urate, adjuvant aluminum, rotenone, live E. coli, anthrax lethal toxin, DNA transfection, and S. Typhimurium infection. PKR deficiency significantly inhibited the secretion of IL-1beta, IL-18 and HMGB1 in E. coli-induced peritonitis. PKR physically interacts with multiple inflammasome components, including NLR family pyrin domain-containing 3 (NLRP3), NLR family pyrin domain-containing 1 (NLRP1), NLR family CARD domain-containing protein 4 (NLRC4), Absent in melanoma 2 (AIM2), and broadly regulates inflammasome activation. PKR autophosphorylation in a cell free system with recombinant NLRP3, ASC and pro-casapse-1 reconstitutes inflammasome activity. These results reveal a critical role of PKR in inflammasome activation, and indicate that it should be possible to pharmacologically target this molecule to treat inflammation.
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              Human tyrosine kinase 2 deficiency reveals its requisite roles in multiple cytokine signals involved in innate and acquired immunity.

              Tsutomu Iwata, Ken-ichi Watanabe, Ayse Metin … (2006)
              Tyrosine kinase 2 (Tyk2) is a nonreceptor tyrosine kinase that belongs to the Janus kinase (Jak) family. Here we identified a homozygous Tyk2 mutation in a patient who had been clinically diagnosed with hyper-IgE syndrome. This patient showed unusual susceptibility to various microorganisms including virus, fungi, and mycobacteria and suffered from atopic dermatitis with elevated serum IgE. The patient's cells displayed defects in multiple cytokine signaling pathways including those for type I interferon (IFN), interleukin (IL)-6, IL-10, IL-12, and IL-23. The cytokine signals were successfully restored by transducing the intact Tyk2 gene. Thus, the Tyk2 deficiency is likely to account for the patient's complex clinical manifestations, including the phenotype of impaired T helper 1 (Th1) differentiation and accelerated Th2 differentiation. This study identifies human Tyk2 deficiency and demonstrates that Tyk2 plays obligatory roles in multiple cytokine signals involved in innate and acquired immunity of humans, which differs substantially from Tyk2 function in mice.
              Article 0 comments Cited 165 times – based on 0 reviews     Review now
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                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 January 2013
                Publication date (Electronic): 01 January 2013
                Publication date PMC-release: 01 January 2013
                Volume: 2
                Issue: 1
                Electronic Location Identifier: e23633
                Affiliations
                Department of Immunology and Department of Molecular Biology; UT Southwestern Medical Center; Dallas, TX USA
                Author notes
                [* ]Correspondence to: J. David Farrar, Email: David.Farrar@ 123456utsouthwestern.edu
                Article
                Publisher ID: 2012JAKS0098R Publisher Item ID: 23633
                DOI: 10.4161/jkst.23633
                PMC ID: 3670274
                PubMed ID: 24058798
                SO-VID: 347188ac-ed36-4395-8fd2-b44d0e30591e
                Copyright © Copyright © 2013 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
                Date received : 26 November 2012
                Date revision received : 11 January 2013
                Date accepted : 15 January 2013
                Categories
                Subject: Special Focus Review

                Keywords: interferon,signal transducer and activator of transcription,stat2,viral antagonism,comparative genomics,interferon stimulated gene
                Data availability:
                Keywords: interferon, signal transducer and activator of transcription, stat2, viral antagonism, comparative genomics, interferon stimulated gene

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