Background Platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR) have been reported to reflect the inflammatory response and disease activity in a variety of autoimmune diseases. Objectives This study aimed to evaluate the value of PLR and NLR as markers to monitor disease activity in Takayasu’s arteritis (TAK). Methods A retrospective case–control study involving 88 patients with TAK and 78 healthy controls was performed. We compared the PLR and NLR between patients and healthy controls, and also analysed the correlations between PLR or NLR and indices of TAK disease activity. Results Increased PLR and NLR were observed in patients with TAK. PLR was positively correlated with hs-C-reactive protein (hs-CRP) (r=0.239, p=0.010) and erythrocyte sedimentation rate (ESR) (r=0.270, p=0.010). NLR also exhibited a positive relationship with Kerr’s score (r=0.284, p=0.002), hs-CRP (r=0.313, p=0.006) and ESR (r=0.249, p=0.019). A PLR level of 183.39 was shown to be the predictive cut-off value for TAK (sensitivity 37.8%, specificity 93.0%, area under the curve (AUC)=0.691). A NLR level of 2.417 was found to be the predictive cut-off value for TAK (sensitivity 75.6%, specificity 55.8%, AUC=0.697). Conclusions PLR and NLR could be useful markers to reflect inflammation and disease activity in patients with TAK.

Purpose: Thoracic aortic dissection (TAD) is characterized by an inflammatory response. Angiopoietin-like protein 8 (ANGPTL8) is a hormone involved in the regulation of lipid metabolism and inflammation. However, the relationship between ANGPTL8 and TAD remains unknown. Methods: This case-control study included 78 TAD patients and 72 controls. The aortic diameter was evaluated by computed tomography and used to assess TAD severity. Circulating ANGPTL8 levels were measured by enzyme-linked immunosorbent assay. Associations of ANGPTL8 with TAD were determined by multivariate logistic regression. Results: Serum ANGPTL8 levels were significantly higher in TAD patients compared with controls (562.50 ± 20.84 vs. 419.70 ± 22.65 pg/mL, respectively; P < 0.001). After adjusting for confounding factors, circulating ANGPTL8 levels were an independent risk factor for TAD (odds ratio = 1.587/100 pg ANGPTL8, 95% confidence interval [CI] = 1.121–2.247, P < 0.001) and positively associated with diameter (β = 1.081/100 pg ANGPTL8, 95% CI = 0.075–2.086, P = 0.035) and high-sensitivity C-reactive protein (hs-CRP) (β = 0.845/100 pg ANGPTL8, 95% CI = 0.020–1.480, P = 0.009). The area under the curve (AUC) on receiver operating characteristic (ROC) analysis of the combination of ANGPTL8, hs-CRP, and D-dimer was 0.927, and the specificity and sensitivity were 98.46% and 79.49%, respectively. ANGPTL8 was significantly increased in TAD tissue compared with controls. In vitro, ANGPTL8 was increased in angiotensin II (AngII)-treated macrophages and vascular smooth muscle cells (VSMCs), while ANGPTL8 siRNA-mediated knockdown decreased inflammatory factors in AngII-treated macrophages and decreased apoptosis in AngII-treated VSMCs. Conclusion: ANGPTL8 is associated with TAD occurrence and development, which may involve pro-inflammatory effects on macrophages. ANGPTL8 combined with D-dimer and hs-CRP might be a useful clinical predictor of TAD. Trial Registration: ChiCTR-COC-17010792 http://www.chictr.org.cn/showproj.aspx?proj=18288

Interferon-gamma (IFN-γ) is a cytokine involved in the pathogenesis of Takayasu’s arteritis (TAK). However, the source of IFN-γ in TAK patients is not fully clear. We aimed to investigate the source of IFN-γ in TAK. 60 TAK patients and 35 health controls were enrolled. The lymphocyte subsets of peripheral blood were detected by flow cytometry, cytokines were detected by Bio-plex. The correlation among lymphocyte subsets, cytokines and disease activity indexes was analyzed by person correlation. The level of serum IFN-γ in TAK patients was significantly increased (P < 0.05). The percentage of CD3⁺IFN-γ⁺ cells in peripheral blood CD3⁺ cells was significantly higher in TAK patients than that of healthy control group (P = 0.002). A higher proportion of CD3⁺CD8⁺IFN-γ⁺ cells/CD3⁺IFN-γ⁺ cells (40.23 ± 11.98% vs 35.12 ± 11.51%, P = 0.049), and a significantly lower CD3⁺CD4⁺IFN-γ⁺/ CD3⁺CD8⁺IFN-γ⁺ ratio (1.34 ± 0.62% vs 1.80 ± 1.33%, P = 0.027) were showed in the TAK group than that of control group. The CD3⁺CD8⁺IFN-γ⁺/CD3⁺IFN-γ⁺ ratio was positively correlated with CD3⁺IFN-γ⁺cells/ CD3⁺cells ratio (r = 0.430, P = 0.001), serum IFN-γ level (r = 0.318, P = 0.040) and IL-17 level (r = 0.326, P = 0.031). It was negatively correlated with CD3⁺CD4⁺IFN-γ⁺/CD3⁺IFN-γ⁺ ratio (r = − 0.845, P < 0.001). IFN-γ secreted by CD3⁺CD8 ⁺ T cells is an important source of serum IFN-γ in TAK patients.