急性胰腺炎是胰腺常见的急性炎症性疾病，其发病率在全球范围内呈上升趋势。大约 10% 的急性胰腺炎会进展为重症急性胰腺炎 (SAP)，其发病率和死亡率很高。对胰腺损伤的免疫反应紊乱被认为是 SAP 中介导全身损伤的关键事件。在本文中，我们回顾了 SAP 免疫生物标志物的最新进展以及未来的研究方向。鉴于 NLRP3 炎症小体通路在介导全身炎症反应综合征和全身损伤中的重要性，最近的研究调查了 SAP 与全身激活剂水平的关系NLRP3，例如首次在人类 SAP 中发现损伤相关分子模式 (DAMP)。例如，组蛋白、线粒体 DNA 和无细胞 DNA 的循环水平与 SAP 相关。一组机械相关的免疫标记物（例如，血管生成素-2、肝细胞生长因子、白介素-8 (IL-8)、抵抗素和 sTNF-α R1 组）比现有的临床评分和个体免疫标记物具有更高的预测准确性。在已确定与 SAP 发病机制相关的细胞因子中，免疫疗法的 2 期试验正在进行中，包括肿瘤坏死因子 (TNF)-α 抑制和刺激 IL-10 产生，以确定改变免疫反应是否可以减轻急性胰腺炎的严重程度(美联社)。各种 DAMP 的循环系统水平和一组可能反映驱动 SAP 的不同途径活动的免疫标记物似乎有望作为 SAP 的预测生物标记物。但需要更大规模的多中心研究来进行外部验证。使用免疫表型分析技术调查驱动 SAP 的免疫细胞途径的研究很少。还需要跨学科的努力，将一些有前途的生物标志物带到床边进行临床实用性的验证和测试。需要研究肠道淋巴和肠道微生物群改变在严重 AP 中的作用和特征。版权所有 © 2024 Wolters Kluwer Health, Inc. 保留所有权利。

Acute pancreatitis is a common acute inflammatory disorder of the pancreas, and its incidence has been increasing worldwide. Approximately 10% of acute pancreatitis progresses to severe acute pancreatitis (SAP), which carries significant morbidity and mortality. Disordered immune response to pancreatic injury is regarded as a key event that mediates systemic injury in SAP. In this article, we review recent developments in immune biomarkers of SAP and future directions for research.Given the importance of the NLRP3-inflammasome pathway in mediating systemic inflammatory response syndrome and systemic injury, recent studies have investigated associations of SAP with systemic levels of activators of NLRP3, such as the damage associated molecular patterns (DAMPs) for the first time in human SAP. For example, circulating levels of histones, mitochondrial DNAs, and cell free DNAs have been associated with SAP. A panel of mechanistically relevant immune markers (e.g., panel of Angiopoeitin-2, hepatocyte growth factor, interleukin-8 (IL-8), resistin and sTNF-α R1) carried higher predictive accuracies than existing clinical scores and individual immune markers. Of the cytokines with established relevance to SAP pathogenesis, phase 2 trials of immunotherapies, including tumor necrosis factor (TNF)-alpha inhibition and stimulation of IL-10 production, are underway to determine if altering the immunologic response can reduce the severity of acute pancreatitis (AP).Circulating systemic levels of various DAMPs and a panel of immune markers that possibly reflect activities of different pathways that drive SAP appear promising as predictive biomarkers for SAP. But larger multicenter studies are needed for external validation. Studies investigating immune cellular pathways driving SAP using immunophenotyping techniques are scarce. Interdisciplinary efforts are also needed to bring some of the promising biomarkers to the bedside for validation and testing for clinical utility. Studies investigating the role of and characterization of altered gut-lymph and gut-microbiota in severe AP are needed.Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.