摘要
After ischemic stroke, proinflammatory molecules known as danger-associated molecular patterns (DAMPs) originating from damaged brain cells recruit and activate immune cells (neutrophils, macrophages, lymphocytes) further eliciting innate and adaptive immunity. During the acute phase from day 1 to day 3 of the stroke onset, macrophages play a major role in the progression of inflammation, promoting the destruction of brain tissue. During the recovery phase, from day 3~4 to day 7 after stroke onset, infiltrating macrophages switch to repairing macrophages, which clear the DAMPs and promote tissue repair by producing neurotrophic factors. Adaptive immunity during the late or chronic phase (> day 7) of stroke has not been well investigated. Recent studies have also indicated that antigen-specific T cells, especially regulatory T cells (Tregs), play major roles in neural repair. This review focuses mainly on the resolution of inflammation and tissue repair by macrophages and Tregs.
基金
This work was supported by JSPS KAKENHI(S)JP17H06175,Challenging Research(P)JP18H05376,and AMED-CREST JP20gm1110009 to Yoshimura A
JSPS KAKENHI 17K15667,19H04817,and 19K16618,AMED-PRIME 20gm6210012 to Ito M and by the Tomizawa Jun-ichi&Keiko Fund of Molecular Biology Society of Japan for Young Scientists,a Research Grant for Young Investigators by The Mitsubishi Foundation
the Mochida Memorial Foundation for Medical and Pharmaceutical Research
the Takeda Science Foundation
the Uehara Memorial Foundation
the Naito Memorial Foundation
the Kanae Foundation
the SENSHIN Medical Research Foundation
the Astellas Foundation for Research on Metabolic Disorders,an Inoue Research Award,a Life Science Research Award,and Keio Gijuku Academic Developmental Funds.
