Li Tengda, Gu Mingli, Liu Peng, Liu Yun, Guo Jie, Zhang Weiwei, Qian Cheng, Deng Anmei
Center of Clinical Experiments, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
Department of Laboratory Diagnosis, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
Microbiol Immunol. 2018 May 26. doi: 10.1111/1348-0421.12605.
In psoriasis, a chronic, recurrent, inflammatory skin disease, CD4+T cells and their related cytokines play an important role in its pathogenesis. The role of interleukin (IL)-35, an immunosuppressive cytokine involved in many autoimmune diseases, is unclear in the pathogenesis of psoriasis. This study evaluated IL-35 expression and clinical significance in psoriasis. Protein and mRNA levels of specified markers were measured by enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (qRT-PCR), respectively. Results showed that plasma IL-35 concentrations were lower in patients with psoriasis than in healthy individuals (Z = -6.525, P < .0001). Ebi3 and p35 showed lower mRNA levels in peripheral blood mononuclear cells from patients with psoriasis than in healthy individuals (Z = -5.078, P < .0001, Z = -2.609, P = .009, respectively). The areas under the receiver-operating characteristic (ROC) curves of IL-35, Ebi3, and p35 for patients with psoriasis versus the control were 0.86, 0.78, and 0.64, respectively. Pearson correlation analysis showed that plasma IL-35 expression negatively correlated with interferon-gamma, tumor necrosis factor-alpha, levels of IL-23, -17, and -22, or the Psoriasis Activity and Severity Index and positively correlated with levels of transforming growth factor beta and IL-10 levels in patients with psoriasis. Summarily, IL-35 might mediate psoriasis pathogenesis by influencing the expression of Th1/Th17/T -related cytokines and might be a putative target in monitoring or treating psoriasis.
银屑病是一种慢性、复发性炎症性皮肤病，CD4 + T细胞及其相关细胞因子在其发病机制中起重要作用。白细胞介素（IL）-35是一种参与多种自身免疫性疾病的免疫抑制细胞因子，其在银屑病发病机制中的作用尚不清楚。本研究评估了IL-35在银屑病中的表达及其临床意义。分别采用酶联免疫吸附测定（ELISA）和实时定量聚合酶链反应（qRT-PCR）检测特定标志物的蛋白质和mRNA水平。结果显示，银屑病患者血浆IL-35浓度低于健康个体（Z = -6.525，P <.0001）。银屑病患者外周血单个核细胞中Ebi3和p35的mRNA水平低于健康个体（分别为Z = -5.078，P <.0001；Z = -2.609，P =.009）。银屑病患者与对照组相比，IL-35、Ebi3和p35的受试者工作特征（ROC）曲线下面积分别为0.86、0.78和0.64。Pearson相关性分析显示，银屑病患者血浆IL-35表达与干扰素-γ、肿瘤坏死因子-α、IL-23、-17和-22水平或银屑病活动和严重程度指数呈负相关，与转化生长因子β水平和IL-10水平呈正相关。综上所述，IL-35可能通过影响Th1/Th17/T相关细胞因子的表达介导银屑病发病机制，可能是监测或治疗银屑病的一个潜在靶点。
