Interleukin‐17 and ischaemic stroke

Zhang, Qiaohui; Liao, Yan; Liu, Zhenquan; Dai, Yajie; Li, Yunxin; Tang, Yu-Wen

doi:10.1111/imm.13265

Cited by 65 publications

(39 citation statements)

References 127 publications

(170 reference statements)

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“…The imbalance between Th1 and Th2 appears to be a key factor in stroke. Increased IL-17 levels and fewer Treg numbers are directly associated with stroke onset [ 55 , 56 ]. In the present study, iPSC-EVs and EA treatment modulated the inflammatory response by promoting Treg response and suppressing Th17 and Th1 responses.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Potential of a Combination of Electroacupuncture and Human iPSC-Derived Small Extracellular Vesicles for Ischemic Stroke

Deng

Wang

Zhang

et al. 2022

Cells

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This paper aimed to explore the roles of the combination of electroacupuncture (EA) and induced pluripotent stem cell-derived small extracellular vesicles (iPSC-EVs) on mice with ischemic stroke and the underlying mechanisms. A focal cerebral ischemia model was established in C57BL/6 mice through middle cerebral artery occlusion (MCAO). After 3 days, neurological impairment and motor function were examined by performing behavioral tests. The infarct volume and neuronal apoptosis were examined using TTC staining and TUNEL assays. Flow cytometry was performed to assess the proliferation of T lymphocytes. The changes in the interleukin (IL)-33/ST2 axis were evaluated by immunofluorescence and Western blotting. The combination of EA and iPSC-EVs treatment ameliorated neurological impairments and reduced the infarct volume and neuronal apoptosis in MCAO mice. EA plus iPSC-EVs suppressed T helper (Th1) and Th17 responses and promoted the regulatory T cell (Treg) response. In addition, EA plus iPSC-EVs exerted neuroprotective effects by regulating the IL-33/ST2 axis and inhibiting the microglia and astrocyte activation. Taken together, the study shows that EA and iPSC-EVs exerted a synergistic neuroprotective effect in MCAO mice, and this treatment may represent a novel potent therapy for ischemic stroke and damage to other tissues.

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Section: Discussionmentioning

confidence: 99%

Therapeutic Potential of a Combination of Electroacupuncture and Human iPSC-Derived Small Extracellular Vesicles for Ischemic Stroke

Deng

Wang

Zhang

et al. 2022

Cells

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“…γδ T cells are the main sources of IL-17a in the context of stroke ( 52 ). Other innate and adaptive immune cells, including Th17 cells, natural killer T (NKT) cells, natural killer (NK) cells, group 3 innate lymphoid cells (ILC3s), and neutrophils have been found to secrete IL-17a as well ( 59 , 60 ). As previously reported, IL-17a-releasing γδ T cells peak on day 3 after the onset of ischemia, and IL-17a seems to have a crucial role in the maturation of brain infarction ( 59 ).…”

Section: The Role Of γδ T Cells In Cerebral Ischemic Strokementioning

confidence: 99%

γδ T Cell in Cerebral Ischemic Stroke: Characteristic, Immunity-Inflammatory Role, and Therapy

et al. 2022

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Gamma-delta (γδ) T cells are a small subset of T cells that are reported to have a proinflammatory role in the pathophysiology of cerebral ischemia stroke (CIS). Upon activation by interleukin-1 beta (IL-1β), IL-23 and IL-18, γδ T cells are stimulated to secrete various cytokines, such as IL-17a, IL-21, IL-22, and interferon-gamma (IFN-γ). In addition, they all play a pivotal role in the inflammatory and immune responses in ischemia. Nevertheless, the exact mechanisms responsible for γδ T cell proinflammatory functions remain poorly understood, and more effective therapies targeting at γδ T cells and cytokines they release remain to be explored, particularly in the context of CIS. CIS is the second most common cause of death and the major cause of permanent disability in adults worldwide. In this review, we focus on the neuroinflammatory and immune functions of γδ T cells and related cytokines, intending to understand their roles in CIS, which may be crucial for the development of novel effective clinical applications.

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“…IS is accompanied by an increased expression of IL-17 and IL-17RC in the serum in association with increased IL-6 and granulocytemonocyte colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) [65]. It is thought that the IL-17-IL-17R pathway plays a key role in secondary poststroke damage via (a) effects on neutrophil infiltration in cerebral parenchyma, thereby promoting damage and thrombosis; (b) effects on tight junctions with blood-brain-barrier (BBB) breakdown and induction of neuronal apoptosis, and (c) synergistic effects with IL-6 [66]. Moreover, a polymorphism of the IL17RC gene is associated with a poorer prognosis of IS [65].…”

Section: These Results Indicate That Altered Expression Of These Pathways and Transcriptional Factors May Lead To Death Due To Ismentioning

confidence: 99%

New Drug Targets to Prevent Death Due to Stroke: A Review Based on Results of Protein-Protein Interaction Network, Enrichment, and Annotation Analyses

Maes

Nikiforov

Plaimas

et al. 2021

IJMS

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This study used established biomarkers of death from ischemic stroke (IS) versus stroke survival to perform network, enrichment, and annotation analyses. Protein-protein interaction (PPI) network analysis revealed that the backbone of the highly connective network of IS death consisted of IL6, ALB, TNF, SERPINE1, VWF, VCAM1, TGFB1, and SELE. Cluster analysis revealed immune and hemostasis subnetworks, which were strongly interconnected through the major switches ALB and VWF. Enrichment analysis revealed that the PPI immune subnetwork of death due to IS was highly associated with TLR2/4, TNF, JAK-STAT, NOD, IL10, IL13, IL4, and TGF-β1/SMAD pathways. The top biological and molecular functions and pathways enriched in the hemostasis network of death due to IS were platelet degranulation and activation, the intrinsic pathway of fibrin clot formation, the urokinase-type plasminogen activator pathway, post-translational protein phosphorylation, integrin cell-surface interactions, and the proteoglycan-integrin extracellular matrix complex (ECM). Regulation Explorer analysis of transcriptional factors shows: (a) that NFKB1, RELA and SP1 were the major regulating actors of the PPI network; and (b) hsa-mir-26-5p and hsa-16-5p were the major regulating microRNA actors. In conclusion, prevention of death due to IS should consider that current IS treatments may be improved by targeting VWF, the proteoglycan-integrin-ECM complex, TGF-β1/SMAD, NF-κB/RELA and SP1.

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Interleukin‐17 and ischaemic stroke

Cited by 65 publications

References 127 publications

Therapeutic Potential of a Combination of Electroacupuncture and Human iPSC-Derived Small Extracellular Vesicles for Ischemic Stroke

Therapeutic Potential of a Combination of Electroacupuncture and Human iPSC-Derived Small Extracellular Vesicles for Ischemic Stroke

γδ T Cell in Cerebral Ischemic Stroke: Characteristic, Immunity-Inflammatory Role, and Therapy

New Drug Targets to Prevent Death Due to Stroke: A Review Based on Results of Protein-Protein Interaction Network, Enrichment, and Annotation Analyses

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