The development of novel therapeutic method by targeting post-ischemic inflammation has been expected, because there are still few effective therapy for ischemic stroke. We have discovered the previously unknown inflammatory mechanisms after ischemic stroke. Our findings indicate that Bruton’s tyrosine kinase (BTK) is essential for the inflammasome activation which produces IL-1β. IL-1β is one of the most important inflammatory cytokines that enlarges infarct volume and exaggerates neurological deficits. Ibrutinib, a BTK inhibitor, can be a therapeutic agent for ischemic stroke by inhibiting inflammasome activation. We propose that the modulation of post-ischemic inflammation and inflammasome activity is a promising therapeutic strategy for ischemic stroke.
Research Area “Elucidation and control of the mechanisms underlying chronic inflammation”
Research Theme “Investigation of immunoregulatory mechanisms in the chronic inflammation after cerebral injuries”
Minako Ito, Takashi Shichita, Masahiro Okada, Ritsuko Komine, Yoshiko Noguchi, Akihiko Yoshimura, and Rimpei Morita1. “Bruton’s tyrosine kinase is essential for NLRP3 inflammasome activation and contributes to ischaemic brain injury”. Nature Communications, Published online 10 June 2015, doi: 10.1038/ncomms8360.
Takashi Shichita, M.D., Ph.D.
Lecturer, Department of Microbiology and Immunology, School of Medicine, Keio University
Akihiko Yoshimura, Ph.D.
Professor, Department of Microbiology and Immunology, School of Medicine, Keio University
Koji Matsuo, Tetsu Kawaguchi, and Shinichi Kato
Life Innovation Group, Department of Innovation Research, JST