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https://www.readbyqxmd.com/read/29667579/intracellular-antibody-signalling-is-regulated-by-phosphorylation-of-the-fc-receptor-trim21
#1
Claire Dickson, Adam J Fletcher, Marina Vaysburd, Ji-Chun Yang, Donna L Mallery, Jingwei Zeng, Christopher M Johnson, Stephen H McLaughlin, Mark Skehel, Sarah Maslen, James Cruickshank, Nicolas Huguenin-Dezot, Jason W Chin, David Neuhaus, Leo C James
Cell surface Fc receptors activate inflammation and are tightly controlled to prevent autoimmunity. Antibodies also simulate potent immune signalling from inside the cell via the cytosolic antibody receptor TRIM21, but how this is regulated is unknown. Here we show that TRIM21 signalling is constitutively repressed by its B-Box domain and activated by phosphorylation. The B-Box occupies an E2 binding site on the catalytic RING domain by mimicking E2-E3 interactions, inhibiting TRIM21 ubiquitination and preventing immune activation...
April 18, 2018: ELife
https://www.readbyqxmd.com/read/29650794/comprehensive-analysis-of-the-mutation-spectrum-in-301-german-als-families
#2
Kathrin Müller, David Brenner, Patrick Weydt, Thomas Meyer, Torsten Grehl, Susanne Petri, Julian Grosskreutz, Joachim Schuster, Alexander E Volk, Guntram Borck, Christian Kubisch, Thomas Klopstock, Daniel Zeller, Sibylle Jablonka, Michael Sendtner, Stephan Klebe, Antje Knehr, Kornelia Günther, Joachim Weis, Kristl G Claeys, Berthold Schrank, Anne-Dorte Sperfeld, Annemarie Hübers, Markus Otto, Johannes Dorst, Thomas Meitinger, Tim M Strom, Peter M Andersen, Albert C Ludolph, Jochen H Weishaupt
OBJECTIVES: Recent advances in amyotrophic lateral sclerosis (ALS) genetics have revealed that mutations in any of more than 25 genes can cause ALS, mostly as an autosomal-dominant Mendelian trait. Detailed knowledge about the genetic architecture of ALS in a specific population will be important for genetic counselling but also for genotype-specific therapeutic interventions. METHODS: Here we combined fragment length analysis, repeat-primed PCR, Southern blotting, Sanger sequencing and whole exome sequencing to obtain a comprehensive profile of genetic variants in ALS disease genes in 301 German pedigrees with familial ALS...
April 12, 2018: Journal of Neurology, Neurosurgery, and Psychiatry
https://www.readbyqxmd.com/read/29619982/sting-dependent-interferon-%C3%AE-1-induction-in-ht29-cells-a-human-colorectal-cancer-cell-line-after-gamma-radiation
#3
Jianzhou Chen, Bostjan Markelc, Jakob Kaeppler, Vivian M L Ogundipe, Yunhong Cao, W Gillies McKenna, Ruth J Muschel
PURPOSE: To investigate the induction of type III interferons (IFNs) in human cancer cells by gamma-rays. METHODS AND MATERIALS: Type III IFN expression in human cancer cell lines after gamma-ray irradiation in vitro was assessed by reverse transcription-quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Signaling pathways mediating type III IFN induction were examined by a variety of means, including immunoblotting, flow cytometry, confocal imaging, and reverse transcription-quantitative polymerase chain reaction...
May 1, 2018: International Journal of Radiation Oncology, Biology, Physics
https://www.readbyqxmd.com/read/29618514/activation-of-stimulator-of-interferon-genes-sting-induces-adam17-mediated-shedding-of-the-immune-semaphorin-sema4d
#4
Kou Motani, Hidetaka Kosako
Stimulator of interferon genes (STING) is an endoplasmic reticulum (ER)-resident membrane protein that mediates cytosolic pathogen DNA-induced innate immunity and inflammatory responses in host defenses. STING is activated by cyclic di-nucleotides and is then translocated to the Golgi apparatus, an event that triggers STING assembly with the downstream enzyme TANK-binding kinase 1 (TBK1). This assembly leads to the phosphorylation of the transcription factor interferon regulatory factor 3 (IRF3), which, in turn, induces expression of type-I interferon (IFN) and chemokine genes...
April 4, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29605155/als-genes-in-the-genomic-era-and-their-implications-for-ftd
#5
REVIEW
Hung Phuoc Nguyen, Christine Van Broeckhoven, Julie van der Zee
Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disease, characterized genetically by a disproportionately large contribution of rare genetic variation. Driven by advances in massive parallel sequencing and applied on large patient-control cohorts, systematic identification of these rare variants that make up the genetic architecture of ALS became feasible. In this review paper, we present a comprehensive overview of recently proposed ALS genes that were identified based on rare genetic variants (TBK1, CHCHD10, TUBA4A, CCNF, MATR3, NEK1, C21orf2, ANXA11, TIA1) and their potential relevance to frontotemporal dementia genetic etiology...
March 28, 2018: Trends in Genetics: TIG
https://www.readbyqxmd.com/read/29581886/trim29-negatively-controls-antiviral-immune-response-through-targeting-sting-for-degradation
#6
Qijie Li, Liangbin Lin, Yanli Tong, Yantong Liu, Jun Mou, Xiaodong Wang, Xiuxuan Wang, Yanqiu Gong, Yi Zhao, Yi Liu, Bo Zhong, Lunzhi Dai, Yu-Quan We, Huiyuan Zhang, Hongbo Hu
Innate immune system is armed by several lines of pattern recognition receptors to sense various viral infection and to initiate antiviral immune response. This process is under a tight control and the negative feedback induced by infection and/or inflammation is critical to maintain immune homoeostasis and to prevent autoimmune disorders, however, the molecular mechanism is not fully understood. Here we report TRIM29, a ubiquitin E3 ligase, functions as an inducible negative regulator of innate immune response triggered by DNA virus and cytosolic DNA...
2018: Cell Discovery
https://www.readbyqxmd.com/read/29559975/tank-binding-kinase-1-dependent-responses-in-health-and-autoimmunity
#7
REVIEW
Cynthia Louis, Chris Burns, Ian Wicks
The pathogenesis of autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) is driven by genetic predisposition and environmental triggers that lead to dysregulated immune responses. These include the generation of pathogenic autoantibodies and aberrant production of inflammatory cytokines. Current therapies for RA and other autoimmune diseases reduce inflammation by targeting inflammatory mediators, most of which are innate response cytokines, resulting in generalized immunosuppression...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29548644/sting-dependent-sensing-does-hiv-actually-care
#8
REVIEW
Christian Krapp, Kasper Jønsson, Martin R Jakobsen
Sensing of DNA is essential for the innate immune system to detect threats, like viruses, intracellular bacteria or cellular DNA damage. At the centre of this conserved mammalian mechanism stands the adaptor protein STING. STING is highly regulated and is part of a complex signalling network. This network depends on the sensors cGAS and IFI16 to detect misplaced DNA in the cytoplasm as well as on the kinase TBK1 and the transcription factor IRF3. The DNA sensing machinery has been implicated in many diseases, among others HIV...
March 9, 2018: Cytokine & Growth Factor Reviews
https://www.readbyqxmd.com/read/29547894/a-novel-transcript-isoform-of-sting-that-sequesters-cgamp-and-dominantly-inhibits-innate-nucleic-acid-sensing
#9
Pei-Hui Wang, Sin-Yee Fung, Wei-Wei Gao, Jian-Jun Deng, Yun Cheng, Vidyanath Chaudhary, Kit-San Yuen, Ting-Hin Ho, Ching-Ping Chan, Yan Zhang, Kin-Hang Kok, Wanling Yang, Chi-Ping Chan, Dong-Yan Jin
STING is a core adaptor in innate nucleic acid sensing in mammalian cells, on which different sensing pathways converge to induce type I interferon (IFN) production. Particularly, STING is activated by 2'3'-cGAMP, a cyclic dinucleotide containing mixed phosphodiester linkages and produced by cytoplasmic DNA sensor cGAS. Here, we reported on a novel transcript isoform of STING designated STING-β that dominantly inhibits innate nucleic acid sensing. STING-β without transmembrane domains was widely expressed at low levels in various human tissues and viral induction of STING-β correlated inversely with IFN-β production...
March 14, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29518743/andrographolide-suppresses-trif-dependent-signaling-of-toll-like-receptors-by-targeting-tbk1
#10
Ah-Yeon Kim, Hyun-Jin Shim, Hyeon-Myeong Shin, Yoo Jung Lee, Hyeonjeong Nam, Su Yeon Kim, Hyung-Sun Youn
Toll-like receptors (TLRs) play a crucial role in danger recognition and induction of innate immune response against bacterial and viral infections. The TLR adaptor molecule, toll-interleukin-1 receptor domain-containing adapter inducing interferon-β (TRIF), facilitates TLR3 and TLR4 signaling, leading to the activation of the transcription factor, NF-κB and interferon regulatory factor 3 (IRF3). Andrographolide, the active component of Andrographis paniculata, exerts anti-inflammatory effects; however, the principal molecular mechanisms remain unclear...
April 2018: International Immunopharmacology
https://www.readbyqxmd.com/read/29514903/caspase-dependent-suppression-of-type-i-interferon-signaling-promotes-kshv-lytic-replication
#11
Tate Tabtieng, Alexei Degterev, Marta M Gaglia
An important component of lytic infection by Kaposi's sarcoma-associated herpesvirus (KSHV) is the ability of the virus to evade the innate immune response, specifically type I interferon (IFN) responses that are triggered by recognition of viral nucleic acids. Inhibition of type I IFN responses by the virus promotes viral replication. Here we report that KSHV uses a caspase-dependent mechanism to block type I IFN, in particular IFNβ, responses during lytic infection. Inhibition of caspases during KSHV reactivation resulted in increased TBK1/IKKϵ-dependent phosphorylation of IRF3 as well as elevated levels of IFNβ transcription and secretion...
March 7, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29503440/tbk1-as-a-regulator-of-autoimmunity-and-antitumor-immunity
#12
Jian-Hong Shi, Xiaoping Xie, Shao-Cong Sun
No abstract text is available yet for this article.
March 5, 2018: Cellular & Molecular Immunology
https://www.readbyqxmd.com/read/29502306/antiviral-effects-and-mechanisms-of-yinhuapinggan-granule-against-h1n1-influenza-virus-infection-in-raw264-7-cells
#13
Hai-Xia Du, Hui-Fen Zhou, Hao-Fang Wan, Jie-Hong Yang, Yi-Yu Lu, Yu He, Hai-Tong Wan
Yinhuapinggan granule (YHPG), a modified prescription based on Ma-Huang-Tang (MHT), is used in traditional Chinese medicine (TCM) to treat influenza, cough, and viral pneumonia. In this study, we investigated the antiviral effects of YHPG by means of pre-, post-, and co-treatment, and its underlying mechanisms on regulating the levels of inflammatory-related cytokines, modulating the mRNA expressions of interferon-stimulated genes in influenza virus-infected murine macrophage cells (RAW264.7), and evaluating the protein expressions of key effectors in the Type I IFN and pattern recognition receptor (PRRs) signaling pathways...
March 3, 2018: Inflammopharmacology
https://www.readbyqxmd.com/read/29496741/attenuation-of-cgas-sting-signaling-is-mediated-by-a-p62-sqstm1-dependent-autophagy-pathway-activated-by-tbk1
#14
Thaneas Prabakaran, Chiranjeevi Bodda, Christian Krapp, Bao-Cun Zhang, Maria H Christensen, Chenglong Sun, Line Reinert, Yujia Cai, Søren B Jensen, Morten K Skouboe, Jens R Nyengaard, Craig B Thompson, Robert Jan Lebbink, Ganes C Sen, Geert van Loo, Rikke Nielsen, Masaaki Komatsu, Lene N Nejsum, Martin R Jakobsen, Mads Gyrd-Hansen, Søren R Paludan
Negative regulation of immune pathways is essential to achieve resolution of immune responses and to avoid excess inflammation. DNA stimulates type I IFN expression through the DNA sensor cGAS, the second messenger cGAMP, and the adaptor molecule STING Here, we report that STING degradation following activation of the pathway occurs through autophagy and is mediated by p62/SQSTM1, which is phosphorylated by TBK1 to direct ubiquitinated STING to autophagosomes. Degradation of STING was impaired in p62-deficient cells, which responded with elevated IFN production to foreign DNA and DNA pathogens...
March 1, 2018: EMBO Journal
https://www.readbyqxmd.com/read/29491406/fc%C3%AE-ri-co-stimulation-converts-human-intestinal-cd103-dendritic-cells-into-pro-inflammatory-cells-through-glycolytic-reprogramming
#15
Ivo S Hansen, Lisette Krabbendam, Jochem H Bernink, Fabricio Loayza-Puch, Willianne Hoepel, Johan A van Burgsteden, Elsa C Kuijper, Christianne J Buskens, Willem A Bemelman, Sebastiaan A J Zaat, Reuven Agami, Gestur Vidarsson, Gijs R van den Brink, Esther C de Jong, Manon E Wildenberg, Dominique L P Baeten, Bart Everts, Jeroen den Dunnen
CD103+ dendritic cells (DC) are crucial for regulation of intestinal tolerance in humans. However, upon infection of the lamina propria this tolerogenic response is converted to an inflammatory response. Here we show that immunoglobulin A (IgA) immune complexes (IgA-IC), which are present after bacterial infection of the lamina propria, are important for the induction of inflammation by the human CD103+ SIRPα+ DC subset. IgA-IC, by recognition through FcαRI, selectively amplify the production of proinflammatory cytokines TNF, IL-1β and IL-23 by human CD103+ DCs...
February 28, 2018: Nature Communications
https://www.readbyqxmd.com/read/29472713/adipose-tissue-tbk1-at-the-crossroad-of-signalling-pathways
#16
Claire Greenhill
No abstract text is available yet for this article.
April 2018: Nature Reviews. Endocrinology
https://www.readbyqxmd.com/read/29445009/human-binge-alcohol-intake-inhibits-tlr4-myd88-and-tlr4-trif-responses-but-not-the-tlr3-trif-pathway-hspa1a-and-pp1-play-selective-regulatory-roles
#17
Sujatha Muralidharan, Arlene Lim, Donna Catalano, Pranoti Mandrekar
Binge/moderate alcohol suppresses TLR4-MyD88 proinflammatory cytokines; however, alcohol's effects on TLR-TRIF signaling, especially after in vivo exposure in humans, are unclear. We performed a comparative analysis of the TLR4-MyD88, TLR4-TRIF, and TLR3-TRIF pathways in human monocytes following binge alcohol exposure. Mechanistic regulation of TLR-TRIF signaling by binge alcohol was evaluated by analyzing IRF3 and TBK1, upstream regulator protein phosphatase 1 (PP1), and immunoregulatory stress proteins HspA1A and XBP-1 in alcohol-treated human and mouse monocytes/macrophages...
February 14, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29444978/an-off-target-effect-of-bx795-blocks-herpes-simplex-virus-type-1-infection-of-the-eye
#18
Dinesh Jaishankar, Abraam M Yakoub, Tejabhiram Yadavalli, Alex Agelidis, Neel Thakkar, Satvik Hadigal, Joshua Ames, Deepak Shukla
Herpes simplex virus type 1 (HSV-1) causes recurrent mucocutaneous lesions in the eye that may advance to corneal blindness. Nucleoside analogs exemplified by acyclovir (ACV) form the primary class of antiherpetic drugs, but this class suffers limitations due to the emergence of viral resistance and other side effects. While studying the molecular basis of ocular HSV-1 infection, we observed that BX795, a commonly used inhibitor of TANK-binding kinase 1 (TBK1), strongly suppressed infection by multiple strains of HSV-1 in transformed and primary human cells, cultured human and animal corneas, and a murine model of ocular infection...
February 14, 2018: Science Translational Medicine
https://www.readbyqxmd.com/read/29441066/tank-binding-kinase-1-tbk1-isoforms-negatively-regulate-type-i-interferon-induction-by-inhibiting-tbk1-irf3-interaction-and-irf3-phosphorylation
#19
Yi Wei Hu, Jie Zhang, Xiao Man Wu, Lu Cao, Pin Nie, Ming Xian Chang
TANK-binding kinase 1 (TBK1) is an important serine/threonine-protein kinase that mediates phosphorylation and nuclear translocation of IRF3, which contributes to induction of type I interferons (IFNs) in the innate antiviral response. In mammals, TBK1 spliced isoform negatively regulates the virus-triggered IFN-β signaling pathway by disrupting the interaction between retinoic acid-inducible gene I (RIG-I) and mitochondria antiviral-signaling protein (MAVS). However, it is still unclear whether alternative splicing patterns and the function of TBK1 isoform(s) exist in teleost fish...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29429998/zdhhc11-modulates-innate-immune-response-to-dna-virus-by-mediating-mita-irf3-association
#20
Ying Liu, Qian Zhou, Li Zhong, Heng Lin, Ming-Ming Hu, Yan Zhou, Hong-Bing Shu, Shu Li
MITA is a central adaptor in innate immune responses to DNA viruses. The mechanisms responsible for recruitment of downstream kinase TBK1 and the transcription factor IRF3 to MITA remains enigmatic. Here we identified ZDHHC11, a member of DHHC palmitoyl transferase family, as a positive regulator of DNA virus-triggered signaling. Overexpression of ZDHHC11 activated the IFN-β promoter, while ZDHHC11-deficiency specifically impaired DNA virus HSV-1-induced transcription of downstream antiviral genes. Zdhhc11-/- mice exhibited lower serum cytokine levels and higher lethality after HSV-1 infection...
February 12, 2018: Cellular & Molecular Immunology
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