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目的:观察慢性心力衰竭患者白细胞介素-35（IL-35）水平和CD14n +单核细胞功能变化。n 方法:连续入组2018年7月至2019年6月在郑州大学第一附属医院心血管内科住院治疗的慢性心力衰竭患者（74例）和健康对照者（29名），清晨空腹采集抗凝外周血20 ml并分离血浆，采用酶联免疫吸附试验（ELISA）法检测血IL-35水平；纯化外周血CD14n +单核细胞，采用实时定量聚合酶链反应法检测CD14n +单核细胞中IL-35受体亚基IL-12Rβ2和gp130 mRNA相对表达量。以IL-35刺激CD14n +单核细胞，与人脐静脉内皮细胞（HUVEC）直接或间接接触培养，采用ELISA法检测上清中细胞因子和颗粒酶B水平，通过检测乳酸脱氢酶水平计算HUVEC死亡比例。比较慢性心力衰竭组和健康对照组间上述指标的差异。n 结果:慢性心力衰竭组的年龄为（59.4±12.1）岁，男性占58.1%（43例）；健康对照组的年龄为（53.9±9.8）岁，男性占65.5%（19名）；慢性心力衰竭组血浆IL-35水平高于健康对照组［（22.89±7.58）mg/L比（16.42±5.47）mg/L，n P<0.001］，gp130 mRNA相对表达量亦然（1.07±0.19比0.98±0.15，n P=0.022）。慢性心力衰竭组CD14n +单核细胞诱导HUEVC死亡比例在直接和间接接触培养中均低于健康对照组（均n P<0.001），分泌颗粒酶B水平低于健康对照组（n P<0.001）。抑制颗粒酶B后CD14n +单核细胞诱导HUVEC死亡比例降低（n P=0.011）。IL-35刺激CD14n +单核细胞后，其诱导HUVEC死亡比例和颗粒酶B分泌水平降低（均n P<0.001）。n 结论:慢性心力衰竭患者血IL-35表达升高，IL-35可通过抑制颗粒酶B分泌诱导CD14n +单核细胞功能不全，进而促进心力衰竭疾病进程。n “,”Objective:To investigate the changes of interleukin-35 (IL-35) level and CD14n +monocytes function in patients with chronic heart failure (CHF).n Methods:A total of 74 patients with CHF who were hospitalized in the Department of Cardiology of the First Affiliated Hospital of Zhengzhou University between July 2018 and June 2019 as well as 29 healthy controls (HC) were continuously enrolled. 20 ml fasting anticoagulant peripheral blood was collected in the morning, and plasma was separated. IL-35 level was measured by ELISA. Peripheral CD14n +monocytes were purified, and the IL-35 receptor subunits (IL-12Rβ2 and gp130 mRNA) relative levels were semi-quantified by real-time PCR. CD14n +monocytes were stimulated with IL-35, and were cultured in direct contact or indirect contact with human umbilical vein endothelial cells (HUVEC). Cytokines and granzyme B secretion in the supernatants was measured by ELISA. The percentage of HUVEC death was calculated by measuring lactate dehydrogenase level. The difference of the above indicators were compared between the CHF group and the HC group.n Results:The age for the CHF group was (59.4±12.1) years, and 58.1% (43 cases) of them were males. The age for the HC group was (53.9±9.8) years, and 65.5% (19 cases) of them were males. The plasma IL-35 level was higher in the CHF group than the HC group ((22.89±7.58) mg/L vs (16.42±5.47) mg/L, n P<0.001). The gp130 mRNA relative level was also higher in the CHF group than the HC group (1.07±0.19 vs 0.98±0.15, n P=0.022). CD14n +monocytes induced HUVEC death in the CHF group was lower in both direct contact and indirect contact culture system than the HC group (both n P<0.001). The granzyme B secretion was also lower in the CHF group than the HC group (n P<0.001). The CD14n +monocytes induced HUVEC death was down-regulated in response to granzyme B inhibition (n P=0.011). Both the CD14n +monocytes induced HUVEC death and the granzyme B secretion were reduced in response to IL-35 stimulation (both n P<0.001).n Conclusion:CHF patients have the elevated IL-35 expression. IL-35 induces CD14n +monocytes dysfunction via the inhibition of granzyme B secretion. This process promoted the progression of heart failure.n