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Showing 1–8 of 8 results
Advanced filters: Author: Takashi Shichita Clear advanced filters

  • Brain cells that die after stroke release intracellular proteins into their environment. Akihiko Yoshimura and his colleagues demonstrate that peroxiredoxin proteins released from dying cells induce inflammatory cytokine expression and drive brain damage after stroke.

    • Takashi Shichita
    • Eiichi Hasegawa
    • Akihiko Yoshimura
    Research
    Nature Medicine
    Volume: 18, P: 911-917

  • Clarification of mechanisms underlying inflammation and neural repair after ischaemic stroke could lead to improved prognosis. In this Review, Shichita et al. discuss the biphasic nature of the post-stroke inflammatory response and the key molecules and cells involved.

    • Takashi Shichita
    • Hiroaki Ooboshi
    • Akihiko Yoshimura
    Reviews
    Nature Reviews Neuroscience
    Volume: 24, P: 299-312

  • Inflammatory cells invade the brain after stroke, but their role in disease has been unclear. Now, Akihiko Yoshimura and colleagues report that a particular population of T cells that express the inflammatory cytokine IL-17 plays a key role in stroke progression: depletion of these cells—even as late as 1 day after stroke—can alleviate brain injury in mice pages 844–846).

    • Takashi Shichita
    • Yuki Sugiyama
    • Akihiko Yoshimura
    Research
    Nature Medicine
    Volume: 15, P: 946-950

  • Tumour-specific T cells can be expandedin vitroand adoptively transferred for therapy, but this strategy is limited by induction of short-lived T cell populations. Here the authors activate Notch signalling in cultured mouse or human T cells, resulting in the production of a long-lived stem cell memory T cell population that can fight tumours in mice.

    • Taisuke Kondo
    • Rimpei Morita
    • Akihiko Yoshimura
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-14

  • The scavenger receptor MSR1 contributes to the clearance of damage-associated molecular patterns (DAMPs) by infiltrating myeloid cells in the post-stroke rodent brain. Myeloid cell MSR1 deficiency impairs clearance and exacerbates stroke-induced impairments, whereas a pharmacological intervention to boost MSR1 expression improves pathological and functional outcomes.

    • Takashi Shichita
    • Minako Ito
    • Akihiko Yoshimura
    Research
    Nature Medicine
    Volume: 23, P: 723-732

  • A subset of Macro-positive macrophages is identified to have immunosuppressive functions in the periportal vein zones of the liver to mediate excessive inflammation, and their effects depend on commensal gut bacteria.

    • Yu Miyamoto
    • Junichi Kikuta
    • Masaru Ishii
    Research
    Nature
    Volume: 629, P: 901-909

  • Activation of inflammasome contributes to several pathologies. Here, the authors show that Bruton’s tyrosine kinase is essential for NLRP3 inflammasome activation, and that blocking it with the FDA-approved inhibitor ibrutinib limits tissue damage in a mouse model of ischaemic stroke.

    • Minako Ito
    • Takashi Shichita
    • Rimpei Morita
    ResearchOpen Access
    Nature Communications
    Volume: 6, P: 1-11