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  1. Article: Innate immune recognition against SARS-CoV-2.

    Yamada, Taisho / Takaoka, Akinori

    Inflammation and regeneration

    2023  Volume 43, Issue 1, Page(s) 7

    Abstract: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative virus of pandemic acute respiratory disease called coronavirus disease 2019 (COVID-19). Most of the infected individuals have asymptomatic or mild symptoms, but some patients ... ...

    Abstract Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative virus of pandemic acute respiratory disease called coronavirus disease 2019 (COVID-19). Most of the infected individuals have asymptomatic or mild symptoms, but some patients show severe and critical systemic inflammation including tissue damage and multi-organ failures. Immune responses to the pathogen determine clinical course. In general, the activation of innate immune responses is mediated by host pattern-recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs) as well as host damage-associated molecular patterns (DAMPs), which results in the activation of the downstream gene induction programs of types I and III interferons (IFNs) and proinflammatory cytokines for inducing antiviral activity. However, the excessive activation of these responses may lead to deleterious inflammation. Here, we review the recent advances in our understanding of innate immune responses to SARS-CoV-2 infection, particularly in terms of innate recognition and the subsequent inflammation underlying COVID-19 immunopathology.
    Language English
    Publishing date 2023-01-26
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2051471-2
    ISSN 1880-9693 ; 0389-4290
    ISSN 1880-9693 ; 0389-4290
    DOI 10.1186/s41232-023-00259-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cancer cells deliver a suppressive cargo.

    Takaoka, Akinori

    Nature immunology

    2018  Volume 19, Issue 3, Page(s) 207–208

    MeSH term(s) Antiviral Agents ; Exosomes ; Humans ; Immunity, Innate ; Neoplasms
    Chemical Substances Antiviral Agents
    Language English
    Publishing date 2018-02-21
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-018-0050-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Regulation of signaling mediated by nucleic acid sensors for innate interferon-mediated responses during viral infection.

    Takaoka, Akinori / Yamada, Taisho

    International immunology

    2019  Volume 31, Issue 8, Page(s) 477–488

    Abstract: Type I and type III interferons are important anti-viral cytokines that are massively induced during viral infection. This dynamic process is regulated by many executors and regulators for efficient eradication of invading viruses and protection from ... ...

    Abstract Type I and type III interferons are important anti-viral cytokines that are massively induced during viral infection. This dynamic process is regulated by many executors and regulators for efficient eradication of invading viruses and protection from harmful, excessive responses. An array of innate sensors recognizes virus-derived nucleic acids to activate their downstream signaling to evoke cytokine responses including interferons. In particular, a cytoplasmic RNA sensor RIG-I (retinoic acid-inducible gene I) is involved in the detection of multiple types of not only RNA viruses but also DNA viruses. Accumulating findings have revealed that activation of nucleic acid sensors and the related signaling mediators is regulated on the basis of post-translational modification such as ubiquitination, phosphorylation and ADP-ribosylation. In addition, long non-coding RNAs (lncRNAs) have been implicated as a new class of regulators in innate signaling. A comprehensive understanding of the regulatory mechanisms of innate sensor activation and its signaling in host-virus interaction will provide a better therapeutic strategy to efficiently control viral infection and maintain immune homeostasis.
    MeSH term(s) Animals ; Humans ; Immunity, Innate/immunology ; Interferons/immunology ; Nucleic Acids/immunology ; Signal Transduction/immunology ; Virus Diseases/immunology
    Chemical Substances Nucleic Acids ; Interferons (9008-11-1)
    Keywords covid19
    Language English
    Publishing date 2019-04-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1013745-2
    ISSN 1460-2377 ; 0953-8178
    ISSN (online) 1460-2377
    ISSN 0953-8178
    DOI 10.1093/intimm/dxz034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Loss of PARP7 Increases Type I Interferon Signaling in EO771 Breast Cancer Cells and Prevents Mammary Tumor Growth by Increasing Antitumor Immunity.

    Rasmussen, Marit / Alvik, Karoline / Kannen, Vinicius / Olafsen, Ninni E / Erlingsson, Linnea A M / Grimaldi, Giulia / Takaoka, Akinori / Grant, Denis M / Matthews, Jason

    Cancers

    2023  Volume 15, Issue 14

    Abstract: PARP7 is a member of the ADP-ribosyltransferase diphtheria toxin-like (ARTD) family and acts as a repressor of type I interferon (IFN) signaling. PARP7 inhibition causes tumor regression by enhancing antitumor immunity, which is dependent on the ... ...

    Abstract PARP7 is a member of the ADP-ribosyltransferase diphtheria toxin-like (ARTD) family and acts as a repressor of type I interferon (IFN) signaling. PARP7 inhibition causes tumor regression by enhancing antitumor immunity, which is dependent on the stimulator of interferon genes (STING) pathway, TANK-binding kinase 1 (TBK1) activity, and cytotoxic CD8
    Language English
    Publishing date 2023-07-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15143689
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Novel rapid method for identifying and quantifying pathogenic bacteria within four hours of blood collection.

    Miyakoshi, Akio / Niimi, Hideki / Ueno, Tomohiro / Wakasugi, Masahiro / Higashi, Yoshitsugu / Miyajima, Yuki / Mori, Masashi / Tabata, Homare / Minami, Hiroshi / Takaoka, Akinori / Hayashi, Atsushi / Yamamoto, Yoshihiro / Kitajima, Isao

    Scientific reports

    2024  Volume 14, Issue 1, Page(s) 1199

    Abstract: Sepsis is life-threatening organ dysfunction and is considered a major cause of health loss. However, since the current biomarkers of sepsis reflect the host's immune response to microorganisms, they would inevitably cause a time-lag. This means that ... ...

    Abstract Sepsis is life-threatening organ dysfunction and is considered a major cause of health loss. However, since the current biomarkers of sepsis reflect the host's immune response to microorganisms, they would inevitably cause a time-lag. This means that there is still no truly reliable biomarker of sepsis. In the present study, we developed a novel method for identifying and quantifying unknown pathogenic bacteria within four hours of sample collection. The most important point of this study is that the novel method can be used to determine the number of bacteria in a sample as a novel biomarker of infectious diseases. Indeed, based on the number of bacteria, we were able to accurately estimate the severity of microbial infection. Furthermore, using the time-dependent changes in the number of bacteria, we were able to monitor the therapeutic effect accurately. The rapid identification and quantification of bacteria may change our approach to medical care.
    MeSH term(s) Humans ; Bacteria ; Sepsis ; Biomarkers
    Chemical Substances Biomarkers
    Language English
    Publishing date 2024-01-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-50864-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: [Immunosenescence: The Forefront of Infection and Trophic Control].

    Maruyama, Mitsuo / Sakamoto, Akihiko / Morita, Yuji / Takaoka, Akinori

    Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan

    2020  Volume 140, Issue 3, Page(s) 391–393

    Abstract: Recently, aging is becoming an important social problem in many developed countries including Japan. It is socially and universally important to unveil the impact of aging and extend healthy life expectancy. Here we show our recent finding that dedicator ...

    Abstract Recently, aging is becoming an important social problem in many developed countries including Japan. It is socially and universally important to unveil the impact of aging and extend healthy life expectancy. Here we show our recent finding that dedicator of cytokinesis 11 (DOCK11, also known as Zizimin2) may be involved in immunosenescence of B cells. DOCK11 was identified as a guanine nucleotide exchange factor for a small GTPase called cell division cycle 42. Expression of DOCK11 is restricted to lymphoid tissues, and becomes downregulated with age. Thus we examined the involvement of DOCK11 in immunosenescence of B-1a B cells as an example. B-1a cells are the main source of antibodies at steady state, and function as the first line of defense against infection. Although DOCK11 was expressed by B-1a cells, the expression levels declined with age. Furthermore, production of anti-pneumococcal immunoglobulin M antibodies was suppressed in aged mice, and was recovered by adoptive transfer with B-1a cells in a DOCK11-dependent manner. Thus DOCK11 may be involved in immunosenescence of B-1a cells.
    MeSH term(s) Aging/immunology ; Animals ; B-Lymphocytes/immunology ; Cytokinesis/immunology ; Gene Expression ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/immunology ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Immunoglobulin M ; Immunosenescence ; Mice ; Nutritional Status ; Streptococcus pneumoniae/immunology
    Chemical Substances Dock11 protein, mouse ; Guanine Nucleotide Exchange Factors ; Immunoglobulin M
    Language Japanese
    Publishing date 2020-02-27
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 200514-1
    ISSN 1347-5231 ; 0031-6903 ; 0372-7750 ; 0919-2085 ; 0919-2131
    ISSN (online) 1347-5231
    ISSN 0031-6903 ; 0372-7750 ; 0919-2085 ; 0919-2131
    DOI 10.1248/yakushi.19-00193-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: FICZ Exposure and Viral Infection in Mice.

    Yamada, Taisho / Takaoka, Akinori

    Bio-protocol

    2017  Volume 7, Issue 1, Page(s) e2096

    Abstract: The aryl hydrocarbon receptor (AHR) is known as a sensor for dioxins that mediates their toxicity, and also has important biophysiological roles such as circadian rhythms, cell differentiation and immune responses. 6-formylindolo(3,2-b)carbazole (FICZ), ... ...

    Abstract The aryl hydrocarbon receptor (AHR) is known as a sensor for dioxins that mediates their toxicity, and also has important biophysiological roles such as circadian rhythms, cell differentiation and immune responses. 6-formylindolo(3,2-b)carbazole (FICZ), which is derived through the metabolism of L-tryptophan by ultraviolet B irradiation, is one of putative physiological ligands for AHR ( Smirnova
    Language English
    Publishing date 2017-01-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.2096
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: In vitro

    Yamada, Taisho / Takaoka, Akinori

    Bio-protocol

    2017  Volume 7, Issue 1, Page(s) e2097

    Abstract: Activation of the aryl hydrocarbon receptor (AHR) by endogenous ligands has been implicated in a variety of physiological processes such as cell cycle regulation, cell differentiation and immune responses. It is reported that tryptophan metabolites, such ...

    Abstract Activation of the aryl hydrocarbon receptor (AHR) by endogenous ligands has been implicated in a variety of physiological processes such as cell cycle regulation, cell differentiation and immune responses. It is reported that tryptophan metabolites, such as kynurenine (Kyn) and 6-formylindolo(3,2-b)carbazole (FICZ), are endogenous ligands for AHR ( Stockinger
    Language English
    Publishing date 2017-01-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.2097
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Novel rapid method for identifying and quantifying pathogenic bacteria within four hours of blood collection

    Akio Miyakoshi / Hideki Niimi / Tomohiro Ueno / Masahiro Wakasugi / Yoshitsugu Higashi / Yuki Miyajima / Masashi Mori / Homare Tabata / Hiroshi Minami / Akinori Takaoka / Atsushi Hayashi / Yoshihiro Yamamoto / Isao Kitajima

    Scientific Reports, Vol 14, Iss 1, Pp 1-

    2024  Volume 10

    Abstract: Abstract Sepsis is life-threatening organ dysfunction and is considered a major cause of health loss. However, since the current biomarkers of sepsis reflect the host’s immune response to microorganisms, they would inevitably cause a time-lag. This means ...

    Abstract Abstract Sepsis is life-threatening organ dysfunction and is considered a major cause of health loss. However, since the current biomarkers of sepsis reflect the host’s immune response to microorganisms, they would inevitably cause a time-lag. This means that there is still no truly reliable biomarker of sepsis. In the present study, we developed a novel method for identifying and quantifying unknown pathogenic bacteria within four hours of sample collection. The most important point of this study is that the novel method can be used to determine the number of bacteria in a sample as a novel biomarker of infectious diseases. Indeed, based on the number of bacteria, we were able to accurately estimate the severity of microbial infection. Furthermore, using the time-dependent changes in the number of bacteria, we were able to monitor the therapeutic effect accurately. The rapid identification and quantification of bacteria may change our approach to medical care.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: BinCARD2 as a positive regulator of interferon response in innate immunity.

    Suzuki, Hiraku / Kameyama, Takeshi / Takaoka, Akinori

    Biochemical and biophysical research communications

    2019  Volume 511, Issue 2, Page(s) 287–293

    Abstract: Innate immunity is a system that recognizes primarily and excludes pathogenic microorganism. MAVS/IPS-1/Cardif/Visa functions as an adapter protein for RIG-I like receptors (RLRs) and plays a key role in the production of antiviral proteins, interferons ( ...

    Abstract Innate immunity is a system that recognizes primarily and excludes pathogenic microorganism. MAVS/IPS-1/Cardif/Visa functions as an adapter protein for RIG-I like receptors (RLRs) and plays a key role in the production of antiviral proteins, interferons (IFNs), for RNA viruses. However, the activation mechanism is not fully understood. Here, we show that BinCARD isoform2 (BinCARD2), carrying CARD domain structure like MAVS, functions in innate immune response. Knockdown of BinCARD2 reduced the RLR ligand-induced expression of IFN-β mRNA and activation of the IFNB promoter. The activation of the IFNB promoter by overexpression of MAVS or TBK1 was suppressed by silencing of BinCARD2, but no effect on IFNB promoter activation by overexpression of TRIF or constitutive activated IRF-3. Furthermore, we confirmed that BinCARD2 protein associated with MAVS but not TBK1 by immunoprecipitation and colocalized with MAVS. Accordingly, we investigated whether BinCARD2 was involved in MAVS activation and showed that siBinCARD2 did not affect RIG-I/MAVS binding but impaired the MAVS oligomerization. Moreover, we infected A549 cells with vesicular stomatitis virus (VSV) and found that induction of IFN-β and IL-6 mRNA after VSV infection was decreased by BinCARD2 knockdown. Thus, these data may suggest that BinCARD2 associates with MAVS to positively modulate the oligomerization in the RIG-I like receptors pathway and activates innate immune response.
    MeSH term(s) Adaptor Proteins, Signal Transducing/immunology ; Apoptosis ; CARD Signaling Adaptor Proteins/immunology ; Cell Line ; Humans ; Immunity, Innate ; Interferon-beta/immunology ; Mitochondrial Membranes/immunology ; Vesicular Stomatitis/immunology ; Vesicular stomatitis Indiana virus/immunology
    Chemical Substances Adaptor Proteins, Signal Transducing ; CARD Signaling Adaptor Proteins ; CARD19 protein, human ; MAVS protein, human ; Interferon-beta (77238-31-4)
    Language English
    Publishing date 2019-02-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2019.02.029
    Database MEDical Literature Analysis and Retrieval System OnLINE

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