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      Th17 Cells and IL-17A in Ischemic Stroke

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          Abstract

          The neurological injury and repair mechanisms after ischemic stroke are complex. The inflammatory response is present throughout stroke onset and functional recovery, in which CD4 + T helper(Th) cells play a non-negligible role. Th17 cells, differentiated from CD4 + Th cells, are regulated by various extracellular signals, transcription factors, RNA, and post-translational modifications. Th17 cells specifically produce interleukin-17A(IL-17A), which has been reported to have pro-inflammatory effects in many studies. Recently, experimental researches showed that Th17 cells and IL-17A play an important role in promoting stroke pathogenesis (atherosclerosis), inducing secondary damage after stroke, and regulating post-stroke repair. This makes Th17 and IL-17A a possible target for the treatment of stroke. In this paper, we review the mechanism of action of Th17 cells and IL-17A in ischemic stroke and the progress of research on targeted therapy.

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          Neuroinflammation: friend and foe for ischemic stroke

          Richard L. Jayaraj, Sheikh Azimullah, Rami Beiram … (2019)
          Stroke, the third leading cause of death and disability worldwide, is undergoing a change in perspective with the emergence of new ideas on neurodegeneration. The concept that stroke is a disorder solely of blood vessels has been expanded to include the effects of a detrimental interaction between glia, neurons, vascular cells, and matrix components, which is collectively referred to as the neurovascular unit. Following the acute stroke, the majority of which are ischemic, there is secondary neuroinflammation that both promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. The proinflammatory signals from immune mediators rapidly activate resident cells and influence infiltration of a wide range of inflammatory cells (neutrophils, monocytes/macrophages, different subtypes of T cells, and other inflammatory cells) into the ischemic region exacerbating brain damage. In this review, we discuss how neuroinflammation has both beneficial as well as detrimental roles and recent therapeutic strategies to combat pathological responses. Here, we also focus on time-dependent entry of immune cells to the ischemic area and the impact of other pathological mediators, including oxidative stress, excitotoxicity, matrix metalloproteinases (MMPs), high-mobility group box 1 (HMGB1), arachidonic acid metabolites, mitogen-activated protein kinase (MAPK), and post-translational modifications that could potentially perpetuate ischemic brain damage after the acute injury. Understanding the time-dependent role of inflammatory factors could help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.
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            IL-17 and Th17 Cells.

            Thomas Korn, Estelle Bettelli, Mohamed Oukka … (2009)
            CD4+ T cells, upon activation and expansion, develop into different T helper cell subsets with different cytokine profiles and distinct effector functions. Until recently, T cells were divided into Th1 or Th2 cells, depending on the cytokines they produce. A third subset of IL-17-producing effector T helper cells, called Th17 cells, has now been discovered and characterized. Here, we summarize the current information on the differentiation and effector functions of the Th17 lineage. Th17 cells produce IL-17, IL-17F, and IL-22, thereby inducing a massive tissue reaction owing to the broad distribution of the IL-17 and IL-22 receptors. Th17 cells also secrete IL-21 to communicate with the cells of the immune system. The differentiation factors (TGF-beta plus IL-6 or IL-21), the growth and stabilization factor (IL-23), and the transcription factors (STAT3, RORgammat, and RORalpha) involved in the development of Th17 cells have just been identified. The participation of TGF-beta in the differentiation of Th17 cells places the Th17 lineage in close relationship with CD4+CD25+Foxp3+ regulatory T cells (Tregs), as TGF-beta also induces differentiation of naive T cells into Foxp3+ Tregs in the peripheral immune compartment. The investigation of the differentiation, effector function, and regulation of Th17 cells has opened up a new framework for understanding T cell differentiation. Furthermore, we now appreciate the importance of Th17 cells in clearing pathogens during host defense reactions and in inducing tissue inflammation in autoimmune disease.
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              Blood-brain barrier dysfunction and recovery after ischemic stroke.

              Xiaoyan Jiang, Anuska Andjelkovic, Ling Zhu … (2018)
              The blood-brain barrier (BBB) plays a vital role in regulating the trafficking of fluid, solutes and cells at the blood-brain interface and maintaining the homeostatic microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the BBB can be disrupted, followed by the extravasation of blood components into the brain and compromise of normal neuronal function. This article reviews recent advances in our knowledge of the mechanisms underlying BBB dysfunction and recovery after ischemic stroke. CNS cells in the neurovascular unit, as well as blood-borne peripheral cells constantly modulate the BBB and influence its breakdown and repair after ischemic stroke. The involvement of stroke risk factors and comorbid conditions further complicate the pathogenesis of neurovascular injury by predisposing the BBB to anatomical and functional changes that can exacerbate BBB dysfunction. Emphasis is also given to the process of long-term structural and functional restoration of the BBB after ischemic injury. With the development of novel research tools, future research on the BBB is likely to reveal promising potential therapeutic targets for protecting the BBB and improving patient outcome after ischemic stroke.
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                Author and article information

                Contributors
                Xiangjian Zhang:
                ORCID: http://orcid.org/0000-0003-0114-1668
                zhang6xj@aliyun.com
                Journal
                Journal ID (nlm-ta): Mol Neurobiol
                Journal ID (iso-abbrev): Mol Neurobiol
                Title: Molecular Neurobiology
                Publisher: Springer US (New York )
                ISSN (Print): 0893-7648
                ISSN (Electronic): 1559-1182
                Publication date (Electronic): 26 October 2023
                Publication date PMC-release: 26 October 2023
                Publication date (Print): 2024
                Volume: 61
                Issue: 4
                Pages: 2411-2429
                Affiliations
                [1 ]Department of Neurology, Second Hospital of Hebei Medical University, ( https://ror.org/015ycqv20) 215 Hepingxi Road, Shijiazhuang, 050000 Hebei China
                [2 ]Hebei Collaborative Innovation Center for Cardio-Cerebrovascular Disease, Shijiazhuang, 050000 Hebei China
                [3 ]Hebei Key Laboratory of Vascular Homeostasis, Shijiazhuang, 050000 Hebei China
                Author information
                http://orcid.org/0000-0003-0114-1668
                Article
                Publisher ID: 3723
                DOI: 10.1007/s12035-023-03723-y
                PMC ID: 10973033
                PubMed ID: 37884768
                SO-VID: c1ff3611-fc84-4667-a13e-696f565840ce
                Copyright © © The Author(s) 2023
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 16 April 2023
                Date accepted : 17 October 2023
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2024

                ScienceOpen disciplines: Neurosciences
                Keywords: ischemic stroke,neuroinflammation,immunomodulation,th17 cells,interleukin-17a
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: ischemic stroke, neuroinflammation, immunomodulation, th17 cells, interleukin-17a

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