Abstract：
Interstitial lung disease (ILD) is a common and fatal manifestation of antisynthetase syndrome (ASS). The aim of this study was to provide new insight into investigate peripheral blood lymphocytes, CD4+ T cells, cytokine levels and their relation to the clinical profile of untreated patients with ASS-ILD. The retrospective study population included thirty patients diagnosed with ASS-ILD and 30 healthy controls (HCs). Baseline clinical and laboratory data were collected for all subjects, including peripheral blood lymphocyte, CD4+ T cell subsets measured by flow cytometry, and serum cytokine levels measured by multiple microsphere flow immunofluorescence. Their correlations with clinical and laboratory findings were analyzed by Pearson\'s or Spearman\'s correlation analysis. In addition, the Benjamini-Hochberg method was used for multiple correction to adjust the p-values. Patients with ASS-ILD had lower CD8+ T cells, higher proportion of Th17 cells and Th17/Treg ratio than HCs. Serum cytokine levels (IL-1β, IL-6, IL-12, IL-17, IL-8, IL-2, IL-4, IL-10, TNF-α and IFN-γ) were higher in patients with ASS-ILD than HCs. Moreover, Th17/Treg ratio was negatively correlated with diffusing capacity of carbon monoxide (DLCO)%. Our study demonstrated abnormalities of immune disturbances in patients with ASS-ILD, characterized by decreased CD8+ T cells and an increased Th17/Treg ratio, due to an increase in the Th17 cells. These abnormalities may be the immunological mechanism underlying the development of ILD in ASS.
摘要：
间质性肺病（ILD）是抗合成酶综合征（ASS）的常见和致命表现。这项研究的目的是为研究外周血淋巴细胞提供新的见解，CD4+T细胞,细胞因子水平及其与未经治疗的ASS-ILD患者临床特征的关系。回顾性研究人群包括30例诊断为ASS-ILD的患者和30例健康对照(HCs)。收集所有受试者的基线临床和实验室数据，包括外周血淋巴细胞,通过流式细胞术测量CD4+T细胞亚群，和通过多重微球流式免疫荧光测量的血清细胞因子水平。通过Pearson或Spearman相关分析与临床和实验室检查结果的相关性。此外,Benjamini-Hochberg方法用于多次校正以调整p值。ASS-ILD患者的CD8+T细胞较低，Th17细胞比例和Th17/Treg比例高于HC。血清细胞因子水平（IL-1β，ASS-ILD患者的IL-6，IL-12，IL-17，IL-8，IL-2，IL-4，IL-10，TNF-α和IFN-γ）高于HC。此外，Th17/Treg比值与一氧化碳（DLCO）％的扩散能力呈负相关。我们的研究表明ASS-ILD患者的免疫紊乱异常，以CD8+T细胞减少和Th17/Treg比率增加为特征，由于Th17细胞的增加。这些异常可能是ASS中ILD发展的免疫学机制。
