However, few studies have focused on the potential correlation between IL-10R1 and human SLE. Two studies have shown no difference in the IL-10R1 expression levels between SLE patients and healthy controls [18,19]; however, the later study also showed that the gene expression pattern was aberrant in immune cells from SLE patients when induced through IL-10R [19]. MLN0128 mouse The major signal transduction pathway for IL-10 is the Janus kinase/signal transducer and activator of transcription (JAK/STAT) system. Binding of IL-10 to the extracellular domain of IL-10R1 activates phosphorylation

of the receptor-associated Janus tyrosine kinases – JAK1 and Tyk2. These kinases then induce the phosphorylation and activation of the transcription factors, mainly signal transducer and activator of transcription 3 (STAT-3) and STAT-1, which translocate to the nucleus, modifying gene expression [16]. In this paper, we investigated the involvement of IL-10R1 in human SLE by examining its expression and learn more signal transduction in different PBMC subsets from SLE patients and healthy controls, and showed that IL-10R1 expression and signalling were down-regulated in CD4+ cells from lupus nephritis (LN) patients. Twenty-eight SLE patients, 24 females and four males, from Shengjing Hospital of China Medical University in Shenyang (China) and fulfilling the American College of Rheumatology revised

classification criteria for lupus [20], were included in the study. Fourteen of the 28 patients were categorized as having lupus nephritis, based on the urine protein and sediment. The mean age was 36 years (range 17–56 years). Lupus

disease activities were assessed using the SLE disease activity index (SLEDAI) [21]. A patient was defined as having active SLE when the SLEDAI score was ≥ 10·0, and was defined otherwise as inactive. The data from SLE patients and healthy controls are shown in Table 1. Fourteen age- and gender-matched healthy hospital employees (mean age 35 years; age range 19–55) were studied in parallel as controls. This study was approved by the ethics committee of China Medical University, and all participating subjects provided their informed consent. The following monoclonal antibodies were used Fenbendazole for the detection of IL-10R1 expression on the surface of different peripheral leucocytes: phycoerythrin (PE)-IL-10R1 [clone 3F9, rat immunoglobulin (Ig)G2aκ], PE-isotype (R35-95, rat IgG2aκ), fluorescein isothiocyanate (FITC)-anti-CD4 (SK3, mouse IgG1), peridinin chlorophyll protein (PerCP)-anti-CD8 (SK1, mouse IgG1), FITC-anti-CD14 (M5E2, mouse IgG2aκ) and FITC-anti-CD19 (HIB19, mouse IgG1κ). All monoclonal antibodies were purchased from BD PharMingen (San Diego, CA, USA). Briefly, fresh whole blood samples were incubated for 30 min at room temperature with monoclonal antibodies.