Department of Emergency Medicine, Changshu Hospital Affiliated to Xuzhou Medical University, Changshu, China.
Department of Emergency Medicine, The First Affiliated Hospital of Suzhou University, Suzhou, China.
J Interferon Cytokine Res. 2022 May;42(5):235-241. doi: 10.1089/jir.2021.0219. Epub 2022 May 9.
The expression and clinical significance of co-stimulator B7-H4 in acute pancreatitis (AP) is still unclear. study showed that the expression of soluble B7-H4 (sB7-H4) and proportions of membrane B7-H4-positive CD14 cells in the peripheral blood mononuclear cells were upregulated in response to stimulation with plasma from AP patients, lipopolysaccharides, or tumor necrosis factor α (TNF-α). sB7-H4 in the plasma of AP patients were positively correlated with interleukin (IL)-6, IL-10, IL-17A, TNF-α, and interferon-γ The areas under the curves (AUCs) of receiver operating characteristic (ROC) curves of plasma sB7-H4 to distinguish the AP patients from healthy donors, the mild AP (MAP) from the moderately severe acute pancreatitis (MSAP)+severe acute pancreatitis (SAP) or the SAP from the MAP+MSAP were 0.78 ( < 0.001) or 0.773 ( < 0.001) or 0.764 ( < 0.001). sB7-H4 in the plasma of patients were positively correlated with the RANSON scores, Bedside Index of Severity of Acute Pancreatitis scores, Marshall scores, and Acute Physiology And Chronic Health Evaluation II scores; and the AUCs of ROC curves of plasma sB7-H4 in the prediction of local complications was 0.726 ( = 0.001). In conclusion, the co-stimulator B7-H4 is involved in the immune response in AP.
B7-H4 在急性胰腺炎（AP）中的表达及其临床意义尚不清楚。研究表明，AP 患者血浆、脂多糖或肿瘤坏死因子-α（TNF-α）刺激后，可溶性 B7-H4（sB7-H4）和外周血单个核细胞中膜 B7-H4 阳性 CD14 细胞的比例上调。AP 患者血浆中的 sB7-H4 与白细胞介素（IL）-6、IL-10、IL-17A、TNF-α和干扰素-γ呈正相关。sB7-H4 区分 AP 患者与健康供体、轻症急性胰腺炎（MAP）与中重度急性胰腺炎（MSAP）+重症急性胰腺炎（SAP）、SAP 与 MAP+MSAP 的受试者工作特征（ROC）曲线下面积（AUC）分别为 0.78（<0.001）或 0.773（<0.001）或 0.764（<0.001）。患者血浆中的 sB7-H4 与 RANSON 评分、床边严重程度急性胰腺炎评分、Marshall 评分和急性生理学和慢性健康评估 II 评分呈正相关；预测局部并发症时，sB7-H4 预测血浆 ROC 曲线的 AUC 为 0.726（=0.001）。总之，共刺激分子 B7-H4 参与 AP 中的免疫反应。
