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Interleukin-23 secreted by activated macrophages drives γδT cell production of interleukin-17 to aggravate secondary injury after intracerebral hemorrhage
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نویسنده
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zhong q. ,zhou k. ,liang q.-l. ,lin s. ,wang y.-c. ,xiong x.-y. ,meng z.-y. ,zhao t. ,zhu w.-y. ,yang y.-r. ,liao m.-f. ,gong q.-w. ,liu l. ,xiong a. ,hao j. ,wang j. ,yang q.-w.
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منبع
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journal of the american heart association - 2016 - دوره : 5 - شماره : 10
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چکیده
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Background-neuroinflammation plays a key role in intracerebral hemorrhage (ich)-induced secondary brain injury,but the specific roles of peripheral inflammatory cells such as macrophages and lymphocytes remain unknown. the purpose of this study was to explore the roles of macrophages,t lymphocytes,and the cytokines they secrete as potential targets for treating secondary brain injury after ich. methods and results-our results showed that peripheral macrophages and t lymphocytes successively infiltrated the brain,with macrophage counts peaking 1 day after ich and t-lymphocyte counts peaking after 4 days. these peaks in cellular infiltration corresponded to increases in interleukin (il)-23 and il-17 expression,respectively. we found that hemoglobin from the hematoma activated il-23 secretion by infiltrating macrophages by inducing the formation of toll-like receptor (tlr) 2/4 heterodimer. this increased il-23 expression stimulated γδt-cell production of il-17,which increased brain edema and neurologic deficits in the model mice as a proinflammatory factor. finally,we found that sparstolonin b (ssnb) could ameliorate brain edema and neurologic deficits in ich model mice via inhibition of tlr2/tlr4 heterodimer formation,and notably,ssnb interacted with myeloid differentiation factor 88 arg196. conclusions-together,our results reveal the importance of the il-23/il-17 inflammatory axis in secondary brain injury after ich and thus provide a new therapeutic target for ich treatment. © 2016 the authors.
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کلیدواژه
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IL-17; IL-23; Intracerebral hemorrhage; Lymphocyte; Macrophage; TLR2; TLR4
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آدرس
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department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, nanjing university of chinese medicine,jiangsu collaborative innovation center of chinese medicinal resources industrialization,nanjing, China, department of anatomy,histology and embryology,chengdu medical college,chengdu, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, department of neurology,xinqiao hospital,the third military medical university,chongqing, China, basic medical college,zhengzhou university,zhengzhou, China, department of neurology,key laboratory of neurorepair and regeneration,tianjin and ministry of education,tianjin neurological institute,tianjin medical university general hospital,tianjin, China, department of anesthesiology/critical care medicine,school of medicine,johns hopkins university,baltimore,md, United States, department of neurology,xinqiao hospital,the third military medical university,chongqing, China
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Authors
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