Elevated levels of interleukin-27 in patients with Sjögren's syndrome

Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disorder characterized by lymphocytic infiltration and progressive destruction of exocrine glands, such as the salivary and lachrymal glands (1). Patients complain of dry eyes and dry mouth. pSS can also induce extraglandular or systemic disorders including interstitial lung disease (ILD) (2, 3). ILD is frequent in patients with pSS. Taouli et al found that the frequency of ILD increased to 50% when thin-section chest computed tomography was used for diagnosis (4). The pathogenesis of the disease is largely unknown and so no effective therapy is available. pSS is thought to be a T-helper (Th)1-dominated disease and type I interferon (IFN) plays a central role in the pathogenesis of pSS. By gene array studies, an increased activation of type I IFN was found in salivary glands of pSS patients (5, 6). One of the main producers of type I IFN is plasmacytoid DC (pDC) (7). The other proinflammatory cytokines found to be important in pSS are interleukin (IL)-12, IL-18, tumour necrosis factor (TNF)-α, and B-cell activating factor (BAFF) (8). IL-12 and IL-18 are closely related to IFN, and work synergistically to drive a Th1 response. IL-27 is a member of the IL-12 family composed of EBV-induced protein 3 (EBI3) and the p28 subunit that signals through a receptor complex composed of IL-27Rα and glycoprotein 130 (gp130) subunits (9). Previous studies have shown that the role of IL-27 in the regulation of immune responses is controversial. Some studies have shown that IL-27 promotes naive T-cell proliferation and initiates Th1 immune responses (10). However, other studies have shown that IL-27 suppresses the expansion of Th17 cells, suggesting an anti-inflammatory function of IL-27 (11). However, at present, our understanding of the role of IL-27 in pSS is limited. The objective of this study was to detect the serum levels of IL-27 in pSS. Serum samples were obtained from 56 patients (54 females, two males; median age 45 years, range 39–70 years) with pSS. In addition, 25 healthy persons (24 females, one male; median age 43 years, range 34–65 years) of matched age and sex served as controls. All pSS patients were diagnosed according to the revised American–European classification, which identifies six criteria (12). The present study was approved by the ethics committee in our institution according to the Declaration of Helsinki and written informed consent was given by all patients. In addition, levels of Sjögren’s syndrome A (SSA), rheumatoid factor (RF), C-reactive protein (CRP), γ-globin, and immunoglobulin (Ig)G were measured in the sera collected (Table 1). ILD was identified on high-resolution computed tomography (HRCT). Diffusing capacity of the lung for carbon monoxide (%DLCO) was obtained for all patients. Serum levels of IL-27 were detected by enzyme-linked immunosorbent assay (ELISA) kits (R&D Systems, Minneapolis, MN, USA) according to the manufacturer’s instructions. Statistical differences were analysed with the Mann–Whitney test and correlation coefficients were determined by the Spearman rank correlation test using SPSS 17.0 and GraphPad 5 software.