Tomaszewski Michał, Styczeń Agnieszka, Krysa Martyna, Michalski Adam, Morawska-Michalska Izabela, Hymos Anna, Wawer Joanna, Rolińska Agnieszka, Rahnama Mansur, Urbanowicz Tomasz, Grywalska Ewelina
Department of Cardiology, Medical University of Lublin, Jaczewskiego 8 Street, 20-954 Lublin, Poland.
Department of Clinical Immunology, Medical University of Lublin, Chodźki 4a Street, 20-093 Lublin, Poland.
Int J Mol Sci. 2024 Dec 16;25(24):13455. doi: 10.3390/ijms252413455.
Pulmonary arterial hypertension (PAH) is a disease characterized by increased pulmonary vascular resistance and right heart failure, with emerging evidence suggesting a key role for immune dysregulation in its pathogenesis. This study aimed to assess the involvement of lymphocytes, particularly regulatory T cells (Tregs), and the expression of immune checkpoint molecules PD-1 and PD-L1 on peripheral blood subpopulations in patients diagnosed with PAH. The study involved 25 patients; peripheral blood mononuclear cells were isolated and subsequently analyzed using flow cytometry to quantify the Treg cell percentage and evaluate PD-1 and PD-L1 expression across the T and B cells. We observed a significantly higher percentage of Tregs in idiopathic PAH (iPAH) patients compared to healthy controls and those with congenital heart disease-associated PAH (CHD-PAH), connective tissue disease-associated PAH (CTD-PAH), and chronic thromboembolic pulmonary hypertension (CTEPH). An overexpression of PD-1 and PD-L1 was found on CD4+ and CD8+ lymphocytes in all PAH groups, particularly in iPAH and CHD-PAH patients. These findings align with previous research highlighting Treg dysfunction and PD-1/PD-L1 overexpression as contributors to PAH pathogenesis. Our results suggest that targeting immune checkpoints and modulating Treg function could represent novel therapeutic strategies for PAH. Future research should focus on validating these biomarkers in larger, independent cohorts and exploring their clinical utility in diagnosing and managing PAH.
肺动脉高压(PAH)是一种以肺血管阻力增加和右心衰竭为特征的疾病,新出现的证据表明免疫失调在其发病机制中起关键作用。本研究旨在评估淋巴细胞,特别是调节性T细胞(Tregs)的参与情况,以及免疫检查点分子PD-1和PD-L1在诊断为PAH的患者外周血亚群上的表达。该研究纳入了25名患者;分离外周血单个核细胞,随后使用流式细胞术进行分析,以量化Treg细胞百分比,并评估T细胞和B细胞上PD-1和PD-L1的表达。我们观察到,与健康对照以及先天性心脏病相关PAH(CHD-PAH)、结缔组织病相关PAH(CTD-PAH)和慢性血栓栓塞性肺动脉高压(CTEPH)患者相比,特发性PAH(iPAH)患者的Tregs百分比显著更高。在所有PAH组的CD4+和CD8+淋巴细胞上均发现PD-1和PD-L1过表达,尤其是在iPAH和CHD-PAH患者中。这些发现与之前的研究一致,之前的研究强调Treg功能障碍和PD-1/PD-L1过表达是PAH发病机制的促成因素。我们的结果表明,靶向免疫检查点和调节Treg功能可能代表PAH的新治疗策略。未来的研究应集中在更大的独立队列中验证这些生物标志物,并探索它们在PAH诊断和管理中的临床应用。