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  1. Article ; Online: Correction

    Haruka Kinosada / Jun-Ichirou Yasunaga / Kazuya Shimura / Paola Miyazato / Chiho Onishi / Tomonori Iyoda / Kayo Inaba / Masao Matsuoka

    PLoS Pathogens, Vol 13, Iss 2, p e

    HTLV-1 bZIP Factor Enhances T-cell Proliferation by Impeding the Suppressive Signaling of Co-inhibitory Receptors.

    2017  Volume 1006228

    Abstract: This corrects the article DOI:10.1371/journal.ppat.1006120.]. ...

    Abstract [This corrects the article DOI:10.1371/journal.ppat.1006120.].
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2017-02-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: HTLV-1 bZIP Factor Enhances T-Cell Proliferation by Impeding the Suppressive Signaling of Co-inhibitory Receptors.

    Haruka Kinosada / Jun-Ichirou Yasunaga / Kazuya Shimura / Paola Miyazato / Chiho Onishi / Tomonori Iyoda / Kayo Inaba / Masao Matsuoka

    PLoS Pathogens, Vol 13, Iss 1, p e

    2017  Volume 1006120

    Abstract: Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. To enhance cell-to-cell transmission of HTLV-1, the virus increases the number of infected cells in vivo. HTLV-1 bZIP factor (HBZ) is ... ...

    Abstract Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. To enhance cell-to-cell transmission of HTLV-1, the virus increases the number of infected cells in vivo. HTLV-1 bZIP factor (HBZ) is constitutively expressed in HTLV-1 infected cells and ATL cells and promotes T-cell proliferation. However, the detailed mechanism by which it does so remains unknown. Here, we show that HBZ enhances the proliferation of expressing T cells after stimulation via the T-cell receptor. HBZ promotes this proliferation by influencing the expression and function of multiple co-inhibitory receptors. HBZ suppresses the expression of BTLA and LAIR-1 in HBZ expressing T cells and ATL cells. Expression of T cell immunoglobulin and ITIM domain (TIGIT) and Programmed cell death 1 (PD-1) was enhanced, but their suppressive effect on T-cell proliferation was functionally impaired. HBZ inhibits the co-localization of SHP-2 and PD-1 in T cells, thereby leading to impaired inhibition of T-cell proliferation and suppressed dephosphorylation of ZAP-70 and CD3ζ. HBZ does this by interacting with THEMIS, which associates with Grb2 and SHP-2. Thus, HBZ interacts with the SHP containing complex, impedes the suppressive signal from PD-1 and TIGIT, and enhances the proliferation of T cells. Although HBZ was present in both the nucleus and the cytoplasm of T cells, HBZ was localized largely in the nucleus by suppressed expression of THEMIS by shRNA. This indicates that THEMIS is responsible for cytoplasmic localization of HBZ in T cells. Since THEMIS is expressed only in T-lineage cells, HBZ mediated inhibition of the suppressive effects of co-inhibitory receptors accounts for how HTLV-1 induces proliferation only of T cells in vivo. This study reveals that HBZ targets co-inhibitory receptors to cause the proliferation of infected cells.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2017-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Resistance of SARS-CoV-2 variants to neutralization by antibodies induced in convalescent patients with COVID-19

    Yu Kaku / Takeo Kuwata / Hasan Md Zahid / Takao Hashiguchi / Takeshi Noda / Noriko Kuramoto / Shashwata Biswas / Kaho Matsumoto / Mikiko Shimizu / Yoko Kawanami / Kazuya Shimura / Chiho Onishi / Yukiko Muramoto / Tateki Suzuki / Jiei Sasaki / Yoji Nagasaki / Rumi Minami / Chihiro Motozono / Mako Toyoda /
    Hiroshi Takahashi / Hiroto Kishi / Kazuhiko Fujii / Tsuneyuki Tatsuke / Terumasa Ikeda / Yosuke Maeda / Takamasa Ueno / Yoshio Koyanagi / Hajime Iwagoe / Shuzo Matsushita

    Cell Reports, Vol 36, Iss 2, Pp 109385- (2021)

    2021  

    Abstract: Summary: Administration of convalescent plasma or neutralizing monoclonal antibodies (mAbs) is a potent therapeutic option for coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, ... ...

    Abstract Summary: Administration of convalescent plasma or neutralizing monoclonal antibodies (mAbs) is a potent therapeutic option for coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, SARS-CoV-2 variants with mutations in the spike protein have emerged in many countries. To evaluate the efficacy of neutralizing antibodies induced in convalescent patients against emerging variants, we isolate anti-spike mAbs from two convalescent COVID-19 patients infected with prototypic SARS-CoV-2 by single-cell sorting of immunoglobulin-G-positive (IgG+) memory B cells. Anti-spike antibody induction is robust in these patients, and five mAbs have potent neutralizing activities. The efficacy of most neutralizing mAbs and convalescent plasma samples is maintained against B.1.1.7 and mink cluster 5 variants but is significantly decreased against variants B.1.351 from South Africa and P.1 from Brazil. However, mAbs with a high affinity for the receptor-binding domain remain effective against these neutralization-resistant variants. Rapid spread of these variants significantly impacts antibody-based therapies and vaccine strategies against SARS-CoV-2.
    Keywords COVID-19 ; SARS-CoV-2 ; neutralizing antibody ; mAb ; variant ; Biology (General) ; QH301-705.5
    Subject code 616
    Language English
    Publishing date 2021-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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