[原发性胆道胆管炎外周血T淋巴细胞亚群特征及临床价值]。

细胞与分子免疫学杂志 Pub Date : 2025-05-01
Liming Zheng, Jinhan Liu, Hong Li, Longgen Liu, Guojun Zheng, Sijia Dai
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引用次数: 0

摘要

目的分析原发性胆道性胆管炎(PBC)患者外周血淋巴细胞亚群及白细胞介素1β(IL-1β)、IL-2、IL-4、IL-5、IL-6、IL-8、IL-10、IL-12P70、IL-17A、肿瘤坏死因子α(TNF-α)、干扰素γ(IFN-γ)、IFN-α等细胞因子水平的变化特点及临床意义,为PBC的发病机制提供新的认识。方法回顾性收集常州市第三人民医院2023年1月1日至2024年6月30日期间主要诊断为PBC的住院患者和健康体检者的临床特征和实验室资料。结果共纳入152例PBC患者和96例健康对照者,符合纳入和排除标准。两组患者的基线特征和实验室数据均有显著差异。经过倾向评分匹配(PSM)分析,61例PBC患者和61例健康对照成功匹配,确保了两组的一般特征(年龄和性别)的平衡和可比性。与对照组相比,PBC组外周血淋巴细胞比例明显升高(31.9% vs. 17.8%),主要原因是CD4+ T细胞增加(46.77% vs. 41.19%),而CD8+T细胞明显降低(19.73% vs. 22.07%)。值得注意的是,CD4+程序性细胞死亡1 (PD-1)+ T和CD8+PD-1+ T细胞比例升高,其中CD8+PD-1+ T细胞与肝脏炎症严重程度呈显著正相关(r=0.41)。此外,PBC患者CD4+ T细胞的线粒体质量(MM)显著增加,而CD8+ T细胞的线粒体质量(MM)和CD3+ T细胞的线粒体膜电位(MMP)没有明显变化。此外,血浆中IL-4、IL-8、IL-10、IFN-α等细胞因子水平异常升高。PBC患者血浆IL-5和IL-1β水平与肝纤维化分期呈负相关(r=-0.52)。结论PBC患者CD4+ T细胞的过度激活和增殖,以及CD8+ T细胞功能的抑制和PD-1表达的升高导致T细胞衰竭,提示PBC患者存在明显的免疫学改变。这些变化与疾病进展密切相关。此外,细胞因子可能参与PBC的免疫调节过程,并可能影响疾病的发病机制。定期监测淋巴细胞亚群和细胞因子水平有助于评估PBC患者的免疫状态和疾病活动性,从而指导个体化治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[The characteristics and clinical values of peripheral T lymphocytic subsets and functional changes in primary biliary cholangitis].

Objective This study aimed to analyze the characteristics and clinical significance of peripheral lymphocytic subsets and cytokine levels, including interleukin 1β(IL-1β), IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12P70, IL-17A, tumor necrosis factor α(TNF-α), interferon γ(IFN-γ) and IFN-α, in patients with primary biliary cholangitis (PBC), to provide some novel insights into the pathogenesis of PBC. Methods We retrospectively collected clinical features and laboratory data from hospitalized patients who were primarily diagnosed with PBC and from healthy physical examinees at the Third People's Hospital of Changzhou between January 1, 2023, and June 30, 2024. Results A total of 152 PBC patients and 96 healthy controls who met the inclusion and exclusion criteria were enrolled. Significant differences were observed in baseline characteristics and laboratory data between the two groups. After the propensity score matching (PSM) analysis, 61 PBC patients and 61 healthy controls were successfully matched, ensuring that the general characteristics (age and gender) of the two groups were balanced and comparable. Compared to the control group, the proportion of peripheral lymphocytes was significantly higher in the PBC group (31.9% vs. 17.8%), primarily due to an increase in CD4+ T cells (46.77% vs. 41.19%), while CD8+T cells were significantly decreased (19.73% vs. 22.07%). Notably, the proportions of CD4+ programmed cell death 1 (PD-1)+ T and CD8+PD-1+ T cells were elevated, with CD8+PD-1+ T cells showing a significant positive correlation with the severity of liver inflammation (r=0.41). Furthermore, the mitochondrial mass (MM) of CD4+ T cells was significantly increased in PBC patients, whereas no significant changes were observed in the MM of CD8+ T cells or the mitochondrial membrane potential (MMP) of CD3+ T cells. Additionally, the plasma levels of cytokines, such as IL-4, IL-8, IL-10 and IFN-α, were abnormally elevated. The plasma levels of IL-5 and IL-1β were negatively correlated with the stage of liver fibrosis in patients with PBC (r=-0.52). Conclusion The overactivation and proliferation of CD4+ T cells, along with the suppression of CD8+ T cell function and increased PD-1 expression leads to T cell exhaustion, indicating significant immunological alterations in PBC patients. These changes are closely associated with the disease progression. Additionally, cytokines are likely involved in the immune regulation process of PBC and may influence the pathogenic mechanisms of the disease. Regular monitoring of lymphocyte subsets and cytokine levels can help assess the immune status and disease activity in patients with PBC, thereby guiding the individualized treatment strategies.

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