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Interleukin‐17 and ischaemic stroke
Author(s) -
Zhang Qiaohui,
Liao Yan,
Liu Zhenquan,
Dai Yajie,
Li Yunxin,
Li Yue,
Tang Yibo
Publication year - 2021
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13265
Subject(s) - stroke (engine) , rheumatoid arthritis , medicine , multiple sclerosis , inflammation , pathological , ischaemic stroke , interleukin 17 , pathophysiology , immunology , immune system , cytokine , receptor , mechanism (biology) , interleukin , interleukin 6 , bioinformatics , ischemia , biology , mechanical engineering , philosophy , epistemology , engineering
IL‐17 family was conducted with 6 members, most of them are widely involved in a variety of acute and chronic inflammatory responses, especially IL‐17A. After stroke, cerebral ischaemia and hypoxia lead nerve cell necrosis and release a large amount of damage‐associated molecular patterns and inflammation factors to activate IL‐17A. Then, IL‐17A promotes the development of stroke by inducing the secretion of inflammatory factors (such as TNF‐α, IL‐6, CXCL1), recruiting neutrophils to infiltrate into central nervous system and impairing the integrity of blood–brain barrier.