Abstract

Background Behcet’s disease(BD) is a chronic systemic vascular inflammatory disease.Autoimmune imbalance associated with genetic and infectious factors promotes the immune response of neutrophils and T cells, which is BD’s important pathogenesis. Several studies indicate the Th17/Treg immune imbalance may play an important role in BD pathogenesis[1-2].Although the proportion of Th17 cells was notably increased, which was accompanied by an increased levels of IL-17, IL-23[1], whether other cytokines are associated with Th17/Treg immune balance is unclear. Objectives The aim of this study was to examine associations between levels of a broad selection of cytokines and Th17/Treg immune balance in patients with BD. Methods The study included 66 BD patients and 66 healthy controls. The absolute counts of lymphocyte subsets and CD4+T cell subsets were detected by flow cytometry for all participants.Serum levels of the following 6 cytokines were determined in the same samples using a cytometric beads array:Interleukin-2(IL-2),Interleukin-4(IL-4), Interleukin-6(IL-6),Interleukin-10(IL-10),Interferon-γ(INF-γ)and Tumor necrosis factor-α(TNF-α) for all BD patients.T tests was used to compare continuous measures.Correlations between levels of cytokines and Th17/Treg were assessed by Spearman’s rank correlation tests. Results (1)Compared to healthy controls, the absolute counts of T cells were increased(P=0.048),the absolute counts of CD8+T cells were also increased (P=0.031) in BD group, the absolute counts of Th1 and Th17 cells were significantly increased(P Conclusion Our research shows that T cell homeostasis perturbation, especially Th1 and Th17 expansion and Th17/Treg immune imbalance,is the cornerstone of BD pathogenesis.These findings suggest that immune responses associated with increased levels of IL-2 and IL-4 may promote Th17/Treg immune imbalance. This also highlights the role of IL-2 and IL-4 in maintaining a balance in the Th17/Treg ratio. Further studies are required to evaluate these preliminary findings in different patient populations and also examine the possible molecular mechanisms behind our observations.

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