Department of Cardiology, Yanbian University Hospital, Juzijie, Yanji, Jilin Province, China.
Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
J Hypertens. 2020 Oct;38(10):1878-1889. doi: 10.1097/HJH.0000000000002456.
: Hypertension is a growing health concern worldwide. Established hypertension is a causative factor of heart failure, which is characterized by increased vascular resistance and intractable uncontrolled blood pressure. Hypertension and heart failure have multiple causes and complex pathophysiology but cellular immunity is thought to contribute to the development of both. Recent studies showed that T cells play critical roles in hypertension and heart failure in humans and animals, with various stimuli leading to the formation of effector T cells that infiltrate the cardiovascular wall. Monocytes/macrophages also accumulate in the cardiovascular wall. Various cytokines (e.g. interleukin-6, interleukin-17, interleukin-10, tumor necrosis factor-α, and interferon-γ) released from immune cells of various subtypes promote vascular senescence and elastic laminal degradation as well as cardiac fibrosis and/or hypertrophy, leading to cardiovascular structural alterations and dysfunction. Recent laboratory evidence has defined a link between inflammation and the immune system in initiation and progression of hypertension and heart failure. Moreover, cross-talk among natural killer cells, adaptive immune cells (T cells and B cells), and innate immune cells (i.e. monocytes, macrophages, neutrophils, and dendritic cells) contributes to end-cardiovasculature damage and dysfunction in hypertension and heart failure. Clinical and experimental studies on the diagnostic potential of T-cell subsets revealed that blood regulatory T cells, CD4 cells, CD8 T cells, and the ratio of CD4 to CD8 T cells show promise as biomarkers of hypertension and heart failure. Therapeutic interventions to suppress activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of cardiovascular failure, including hypertension of heart failure.
高血压是全球日益严重的健康问题。已确立的高血压是心力衰竭的一个致病因素，其特征是血管阻力增加和难以控制的血压。高血压和心力衰竭有多种原因和复杂的病理生理学，但细胞免疫被认为有助于两者的发展。最近的研究表明，T 细胞在人类和动物的高血压和心力衰竭中发挥着关键作用，各种刺激导致效应 T 细胞的形成，这些细胞渗透到心血管壁中。单核细胞/巨噬细胞也在心血管壁中积聚。各种细胞因子（如白细胞介素-6、白细胞介素-17、白细胞介素-10、肿瘤坏死因子-α和干扰素-γ）从各种亚型的免疫细胞释放出来，促进血管衰老和弹性层降解以及心脏纤维化和/或肥大，导致心血管结构改变和功能障碍。最近的实验室证据已经确定了炎症和免疫系统在高血压和心力衰竭的发生和进展之间的联系。此外，自然杀伤细胞、适应性免疫细胞（T 细胞和 B 细胞）和固有免疫细胞（即单核细胞、巨噬细胞、中性粒细胞和树突状细胞）之间的串扰导致高血压和心力衰竭中的终末心血管损伤和功能障碍。关于 T 细胞亚群诊断潜力的临床和实验研究表明，血液调节性 T 细胞、CD4 细胞、CD8 T 细胞以及 CD4 与 CD8 T 细胞的比值有望成为高血压和心力衰竭的生物标志物。抑制这些细胞激活的治疗干预可能有助于减少终末器官损伤并预防心血管衰竭的后果，包括心力衰竭的高血压。
