Elevated circulating levels of the interferon-γ-induced chemokines are associated with disease activity and cutaneous manifestations in adult-onset Still's disease.
Elevated circulating levels of the interferon-γ-induced chemokines are associated with disease activity and cutaneous manifestations in adult-onset Still's disease.
复制标题
DOI：
10.1038/srep46652
复制
发表时间：
2017-04-24
影响因子：
4.6
通讯作者：
Kim HA
中科院分区：
文献类型：
--
作者：
Han JH;Suh CH;Jung JY;Ahn MH;Han MH;Kwon JE;Yim H;Kim HA
C-X-C基序趋化因子9 （CXCL9）、CXCL10和CXCL11是响应干扰素-γ (IFN-γ)而产生的，并随着活化淋巴细胞的积累而引发炎症。这些趋化因子可能在成人发病斯蒂尔氏病（AOSD）的发病机制中发挥作用。因此，我们研究了这些趋化因子水平与活动性AOSD患者临床表现之间的关系。采用酶联免疫吸附法测定血清中IFN-γ、CXCL9、CXCL10和CXCL11的水平。AOSD患者的IFN-γ水平高于类风湿关节炎（RA）患者（p = 0.001）或健康对照（hc） （p = 0.032）。AOSD患者的CXCL9、CXCL10和CXCL11水平也高于RA患者（p < 0.001）和hcc患者（p < 0.001）。在接受皮质类固醇治疗的AOSD患者中，CXCL9、CXCL10和CXCL11水平显著下降，而IFN-γ水平无显著差异。免疫组化显示，AOSD患者皮肤活检样本中cxcl10阳性炎症细胞的百分比高于正常对照组（p = 0.012）、湿疹组（p = 0.019）和牛皮癣组（p = 0.009）。IFN-γ诱导的趋化因子CXCL9、CXCL10和CXCL11水平升高，并与几种疾病活动标志物相关。这些干扰素γ诱导的趋化因子可能有助于AOSD的炎症反应和皮肤表现。
C-X-C motif chemokine 9 (CXCL9), CXCL10, and CXCL11 are produced in response to interferon-γ (IFN-γ) and trigger inflammation with the accumulation of activated lymphocytes. It appears that these chemokines could play a role in the pathogenesis of adult-onset Still’s disease (AOSD). Therefore, we investigated the associations between the levels of these chemokine and clinical manifestations in patients with active AOSD. Serum levels of IFN-γ, CXCL9, CXCL10 and CXCL11 were determined using enzyme-linked immunosorbent assays. IFN-γ levels were higher in AOSD patients than in rheumatoid arthritis (RA) patients (p = 0.001) or healthy controls (HCs) (p = 0.032). AOSD patients also exhibited higher levels of CXCL9, CXCL10, and CXCL11 compared with RA patients (p < 0.001) and HCs (p < 0.001). In follow-up AOSD patients after treatment with corticosteroid, the levels of CXCL9, CXCL10 and CXCL11 fell significantly, whereas IFN-γ levels were not significantly different. On immunohistochemistry, the percentage of CXCL10-positive inflammatory cells was higher in skin biopsy samples from AOSD patients than in those from normal control (p = 0.012), eczema (p = 0.019), and psoriasis (p = 0.009) groups. Levels of the IFN-γ–induced chemokines, CXCL9, CXCL10 and CXCL11, were elevated and correlated with several disease activity markers. These interferon-γ–induced chemokines may contribute to inflammatory responses and skin manifestations in AOSD.