title: Imbalance between IL-17A-producing cells and regulatory T cells during ischemic stroke.
abstract: Immune responses and inflammation are key elements in the pathogenesis of ischemic stroke (IS). Although the involvement of IL-17A in IS has been demonstrated using animal models, the involvement of IL-17A and IL-17-secreting T cell subsets in IS patients has not been verified, and whether the balance of Treg/IL-17-secreting T cells is altered in IS patients remains unknown. In the present study, we demonstrated that the proportion of peripheral Tregs and the levels of IL-10 and TGF- β were reduced in patients with IS compared with controls using flow cytometry (FCM), real-time PCR, and ELISA assays. However, the proportions of Th17 and γ δ T cells, the primary IL-17A-secreting cells, increased dramatically, and these effects were accompanied by increases in the levels of IL-17A, IL-23, IL-6, and IL-1 β in IS patients. These studies suggest that the increase in IL-17A-producing cells and decrease in Treg cells might contribute to the pathogenesis of IS. Manipulating the balance between Tregs and IL-17A-producing cells might be helpful for the treatment of IS.
authors.affiliation: Department of Neurology, Southwest Hospital, Third Military Medical University, Institute of Interventional Cerebrovascular Disease, Chongqing 400038, China.
authors.forename: Yuehua
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Department of Pathology and Experimental Medicine, 306 Hospital of PLA, Beijing 100101, China.
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Zheng
authors.affiliation: Department of Neurology, Southwest Hospital, Third Military Medical University, Institute of Interventional Cerebrovascular Disease, Chongqing 400038, China.
authors.forename: Ya
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Institute of Immunology PLA, Third Military Medical University, Chongqing 400038, China.
authors.forename: Bing
authors.identifier: 0000-0002-4297-5346
authors.initials: B
authors.lastname: Ni
authors.affiliation: Department of Neurology, Southwest Hospital, Third Military Medical University, Institute of Interventional Cerebrovascular Disease, Chongqing 400038, China.
authors.forename: Shugui
authors.initials: S
authors.lastname: Shi
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000235:genetics; D006801:Humans; D020381:Interleukin-17 / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D053759:Interleukin-23 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D020521:Stroke / Q000097:blood / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism*
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D015850:Interleukin-6; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3