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{"title":"Actions of Dendritic Cells in the Kidney during Hypertension.","authors":"Xiaohan Lu, Steven D Crowley","doi":"10.1002/cphy.c210050","DOIUrl":null,"url":null,"abstract":"<p><p>The immune response plays a critical role in the pathogenesis of hypertension, and immune cell populations can promote blood pressure elevation via actions in the kidney. Among these cell lineages, dendritic cells (DCs), the most potent antigen-presenting cells, play a central role in regulating immune response during hypertension and kidney disease. DCs have different subtypes, and renal DCs are comprised of the CD103<sup>+</sup> CD11b<sup>-</sup> and CD103<sup>-</sup> CD11b<sup>+</sup> subsets. DCs become mature and express costimulatory molecules on their surface once they encounter antigen. Isolevuglandin-modified proteins function as antigens to activate DCs and trigger them to stimulate T cells. Activated T cells accumulate in the hypertensive kidney, release effector cytokines, promote renal oxidative stress, and promote renal salt and water retention. Individual subsets of activated T cells can secrete tumor necrosis factor-alpha, interleukin-17A, and interferon-gamma, each of which has augmented the elevation of blood pressure in hypertensive models by enhancing renal sodium transport. Fms-like tyrosine kinase 3 ligand-dependent classical DCs are required to sustain the full hypertensive response, but C-X<sub>3</sub> -C chemokine receptor 1 positive DCs do not regulate blood pressure. Excess sodium enters the DC through transporters to activate DCs, whereas the ubiquitin editor A20 in dendritic cells constrains blood pressure elevation by limiting T cell activation. By contrast, activation of the salt sensing kinase, serum/glucocorticoid kinase 1 in DCs exacerbates salt-sensitive hypertension. This article discusses recent studies illustrating mechanisms through which DC-T cell interactions modulate levels of pro-hypertensive mediators to regulate blood pressure via actions in the kidney. © 2022 American Physiological Society. Compr Physiol 12:1-15, 2022.</p>","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":null,"pages":null},"PeriodicalIF":4.2000,"publicationDate":"2022-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Comprehensive Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/cphy.c210050","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
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Abstract
The immune response plays a critical role in the pathogenesis of hypertension, and immune cell populations can promote blood pressure elevation via actions in the kidney. Among these cell lineages, dendritic cells (DCs), the most potent antigen-presenting cells, play a central role in regulating immune response during hypertension and kidney disease. DCs have different subtypes, and renal DCs are comprised of the CD103+ CD11b- and CD103- CD11b+ subsets. DCs become mature and express costimulatory molecules on their surface once they encounter antigen. Isolevuglandin-modified proteins function as antigens to activate DCs and trigger them to stimulate T cells. Activated T cells accumulate in the hypertensive kidney, release effector cytokines, promote renal oxidative stress, and promote renal salt and water retention. Individual subsets of activated T cells can secrete tumor necrosis factor-alpha, interleukin-17A, and interferon-gamma, each of which has augmented the elevation of blood pressure in hypertensive models by enhancing renal sodium transport. Fms-like tyrosine kinase 3 ligand-dependent classical DCs are required to sustain the full hypertensive response, but C-X3 -C chemokine receptor 1 positive DCs do not regulate blood pressure. Excess sodium enters the DC through transporters to activate DCs, whereas the ubiquitin editor A20 in dendritic cells constrains blood pressure elevation by limiting T cell activation. By contrast, activation of the salt sensing kinase, serum/glucocorticoid kinase 1 in DCs exacerbates salt-sensitive hypertension. This article discusses recent studies illustrating mechanisms through which DC-T cell interactions modulate levels of pro-hypertensive mediators to regulate blood pressure via actions in the kidney. © 2022 American Physiological Society. Compr Physiol 12:1-15, 2022.
树突状细胞在高血压患者肾脏中的作用。
免疫反应在高血压的发病机制中起着关键作用,免疫细胞群可以通过肾脏的作用促进血压升高。在这些细胞系中,树突状细胞(dc)是最有效的抗原呈递细胞,在高血压和肾脏疾病期间的免疫反应调节中发挥核心作用。dc有不同的亚型,肾dc由CD103+ CD11b-和CD103- CD11b+亚群组成。树突状细胞一旦遇到抗原,就会成熟并在其表面表达共刺激分子。异黑素修饰的蛋白作为抗原激活dc并触发它们刺激T细胞。活化的T细胞在高血压肾内积聚,释放效应细胞因子,促进肾氧化应激,促进肾盐和水潴留。活化T细胞的单个亚群可以分泌肿瘤坏死因子- α、白细胞介素- 17a和干扰素- γ,每一种都通过增强肾钠转运来增加高血压模型中的血压升高。fms样酪氨酸激酶3配体依赖的经典dc需要维持完全的高血压反应,但C-X3 -C趋化因子受体1阳性dc不能调节血压。过量的钠通过转运体进入DC激活DC,而树突状细胞中的泛素编辑器A20通过限制T细胞激活来限制血压升高。相比之下,DCs中盐敏感激酶、血清/糖皮质激素激酶1的激活会加剧盐敏感性高血压。本文讨论了最近的研究,阐明了DC-T细胞通过相互作用调节促高血压介质的水平,从而通过肾脏调节血压的机制。©2022美国生理学会。物理学报(英文版),2012。
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