Targeting regulatory T cells for cardiovascular diseases

Wang, Xinting; Zhou, Hua; Liu, Qian; Cheng, Peipei; Zhao, Tingyao; Yang, Tianshu; Zhao, Yue; Sha, Wanjing; Zhao, Yihua; Qu, Huiyan

doi:10.3389/fimmu.2023.1126761

Cited by 9 publications

(6 citation statements)

References 223 publications

(109 reference statements)

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“…Interferon-G + T-cells correlated with the NYHA functional class and serum brain natriuretic peptide levels in outpatients with heart failure [30]. Treg acts to resolve inflammation by secreting anti-inflammatory interleukin-10 [31] and inhibiting the activity of effector cells, including Th1 and macrophages [31,32]. In rodent models with angiotensin II infusion [33] or abdominal aortic constriction [24], the adoptive transfer of Treg reduced myocardial infiltration through macrophages and ameliorated cardiac hypertrophy and fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction

Овчинников

Filatova

Потехина

et al. 2023

JCDD

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(1) Background: Chronic inflammation and fibrosis are key players in cardiac remodeling associated with left ventricular hypertrophy (LVH) and heart failure with a preserved ejection fraction (HFpEF). Monocytes and T-helpers (Th) are involved in both pro-inflammatory and fibrotic processes, while regulatory T-cells (Treg) could be considered to suppress chronic inflammation in the hypertrophied myocardium. We aimed to estimate the relationship between the frequencies of circulating CD4+ T-cell and monocyte subpopulations and the variables of left ventricular (LV) diastolic function in patients with LVH depending on the presence of HFpEF. (2) Methods: We enrolled 57 patients with asymptomatic hypertensive LVH (n = 21), or LVH associated with HFpEF (n = 36). A clinical assessment and echocardiographs were analyzed. CD4+ Treg, activated Th (Th-act), and monocyte (classical, intermediate, and non-classical) subpopulations were evaluated via direct immunofluorescence and flow cytometry. (3) Results: Patients with HFpEF had a lower Treg/Th-act ratio (p = 0.001). Though asymptomatic patients and patients with HFpEF were comparable in terms of both the total monocyte number and monocyte subsets, there were moderate correlations between intermediate monocyte count and conventional and novel echocardiographic variables of LV diastolic dysfunction in patients with HFpEF. (4) Conclusions: In patients with LVH, the clinical deterioration (transition to HFpEF) and progression of LV diastolic dysfunction are probably associated with T-cell disbalance and an increase in intermediate monocyte counts.

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Section: Discussionmentioning

confidence: 99%

Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction

Овчинников

Filatova

Потехина

et al. 2023

JCDD

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“…There is precedence for this theory, with publications on several cardiovascular and autoimmune diseases reporting an association between reduced Treg-to-effector T-cell ratio and pathologic in ammation. [53][54][55] This imbalance between the number of Tregs and the number of effector immune cells in in ammation(+) CS parenchyma is only revealed because of the spatial expression methods employed in this experiment. Non-spatially resolved expression methods which would 'average' the Treg expression across the tissue, would miss such subtleties in regional expression.…”

Section: Heterogeneous Immune Pro Les Of Granulomas In Csmentioning

confidence: 94%

Beyond the Granuloma: New Insights into Cardiac Sarcoidosis Using Spatial Proteomics

Peyster,

Smith,

Bittermann

et al. 2024

Preprint

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Cardiac sarcoidosis is poorly understood, challenging to diagnose, and portends a poor prognosis. A lack of animal models necessitates the use of residual human samples to study sarcoidosis, which in turn necessitates the use of analytical tools compatible with archival, fixed tissue. We employed high-plex spatial protein analysis within a large cohort of archival human cardiac sarcoidosis and control tissue samples, studying the immunologic, fibrotic, and metabolic landscape of sarcoidosis at different stages of disease, in different cardiac tissue compartments, and in tissue regions with and without overt inflammation. Utilizing a small set of differentially expressed protein biomarkers, we also report the development of a predictive model capable of accurately discriminating between control cardiac tissue and sarcoidosis tissue, even when no histologic evidence of sarcoidosis is present. This finding has major translational implications, with the potential to markedly improve the diagnostic yield of clinical biopsies obtained from suspected sarcoidosis patients.

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“…Moreover, they have been observed to secrete signals that inhibit fibrosis ( Tang et al, 2012 ); however, the precise characteristics of these signals have yet to be elucidated. Notably, T regs can secrete fibrous mediators, such as TGF-β ( Taylor et al, 2006 ; Saxena et al, 2014 ; Wang et al, 2023 ). Hence, the regulatory role of these cells in the fibrotic response is likely dependent on the specific circumstances and the balance between fibrotic and anti-fibrotic cellular processes.…”

Section: Contribution Of the Immune System To Cardiac Homeostasismentioning

confidence: 99%

Cardiac fibrogenesis: an immuno-metabolic perspective

Hoque,

Gbadegoye,

Hassan

et al. 2024

Front. Physiol.

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Cardiac fibrosis is a major and complex pathophysiological process that ultimately culminates in cardiac dysfunction and heart failure. This phenomenon includes not only the replacement of the damaged tissue by a fibrotic scar produced by activated fibroblasts/myofibroblasts but also a spatiotemporal alteration of the structural, biochemical, and biomechanical parameters in the ventricular wall, eliciting a reactive remodeling process. Though mechanical stress, post-infarct homeostatic imbalances, and neurohormonal activation are classically attributed to cardiac fibrosis, emerging evidence that supports the roles of immune system modulation, inflammation, and metabolic dysregulation in the initiation and progression of cardiac fibrogenesis has been reported. Adaptive changes, immune cell phenoconversions, and metabolic shifts in the cardiac nonmyocyte population provide initial protection, but persistent altered metabolic demand eventually contributes to adverse remodeling of the heart. Altered energy metabolism, mitochondrial dysfunction, various immune cells, immune mediators, and cross-talks between the immune cells and cardiomyocytes play crucial roles in orchestrating the transdifferentiation of fibroblasts and ensuing fibrotic remodeling of the heart. Manipulation of the metabolic plasticity, fibroblast–myofibroblast transition, and modulation of the immune response may hold promise for favorably modulating the fibrotic response following different cardiovascular pathological processes. Although the immunologic and metabolic perspectives of fibrosis in the heart are being reported in the literature, they lack a comprehensive sketch bridging these two arenas and illustrating the synchrony between them. This review aims to provide a comprehensive overview of the intricate relationship between different cardiac immune cells and metabolic pathways as well as summarizes the current understanding of the involvement of immune–metabolic pathways in cardiac fibrosis and attempts to identify some of the previously unaddressed questions that require further investigation. Moreover, the potential therapeutic strategies and emerging pharmacological interventions, including immune and metabolic modulators, that show promise in preventing or attenuating cardiac fibrosis and restoring cardiac function will be discussed.

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Targeting regulatory T cells for cardiovascular diseases

Cited by 9 publications

References 223 publications

Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction

Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction

Beyond the Granuloma: New Insights into Cardiac Sarcoidosis Using Spatial Proteomics

Cardiac fibrogenesis: an immuno-metabolic perspective

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