Background Antiphospholipid syndrome (APS) is an autoimmune disease characterized mainly by recurrent pregnancy failures and/or thrombosis 1. Interleukin (IL)-35, a new member of IL-12 family, was demonstrated to play a role in the immunopathogenesis of several autoimmune diseases 2,3. The expression of IL-35 was observed to be abnormal in idiopathic recurrent pregnancy loss 4.
Objectives To determine the expression of IL-35 and assess its association with clinical /laboratory features in patients with APS.
Methods Serum IL-35 was detected by the enzyme-linked immunosorbent assay (ELISA). 126 patients with APS, 38 patients with primary pregnancy morbidity, and 69 healthy controls were enrolled in the study. Clinical and laboratory features of APS patients were recorded. The Mann-Whitney U test was used to evaluate differences of non-normal distribution data and the Student's t test was used for normal distribution data. The differences in the frequency of clinical /laboratory characteristics were assessed by the Chi-square (χ2) test. The relevances between IL-35 and clinical/laboratory features were further analyzed by the Spearman test (measurement data) or Chi-square (χ2) test (qualitative data).
Results Serum IL-35 was significantly decreased in APS patients (median 14.73, IQR 0–28.09 pg/ml) and patients with primary pregnancy morbidity (16.00, 10.56–25.00 pg/ml), compared to healthy controls (28.87, 20.16–47.47 pg/ml; all p<0.001). Female APS patients with decreased IL-35 had higher risk of pregnancy morbidity than those with normal IL-35, with an odds ratio (OR) of 2.565 (95% confidence interval (CI) 1.138–5.785, p=0.022), especially events of fetus death ≥ the 10th week (OR=6.545, 95% CI 6.03–21.101; p<0.001). In contrast, the frequency of thrombosis was significantly lower in APS patients with decreased IL-35 and the OR value was 0.382 (0.185- 0.789; p=0.009).
Conclusions Serum IL-35 was decreased in APS patients and was associated with pregnancy morbidity and thrombosis, raising the hypothesis of its complicated pathogenic roles in APS.
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Acknowledgement This study was funded by the 973 program of China (No. 2012CB517702) and National Natural Science Foundation of China (No. 81471536). We thank all co-authors for their contribution to this work. We also thank all patients and healthy donors whom took part in this study.
Disclosure of Interest None declared