Peripheral blood of 52 healthy volunteers who had normal physical examinations was collected in May 2015 as control subjects

Peripheral blood of 52 healthy volunteers who had normal physical examinations was collected in May 2015 as control subjects. the formation of immune complexes. Its main manifestations include hypergammaglobulinemia, immune complex formation, and activation of complement system. SLE autoantibodies have a highly specific reaction against autoantigens [1]. Furthermore, abnormal activation of immune cells in SLE patients occurs in T cells and antigen-presenting cells (APC), leading to immune disorders [2]. Signal transduction between immunocompetent cells is accomplished by the activation of intracellular costimulatory molecules. There are two major signaling pathways engaged in T cell activation: one is the response of T cell receptors (TCRs) to an antigen; the other is the stimulation of costimulatory molecules and their receptors. The second signal (signal 2) is provided by the interaction between APC and T cell costimulatory molecules. The positive costimulatory molecules (e.g., CD28, ICOS, ICAM-1, and LFA-3) and the negative costimulatory molecules (e.g., CTLA4, BTLA, and PD-1) form a complex signaling network to comprehensively regulate the immune reaction and play key roles in maintaining appropriate balance of immune activation and tolerance [3, 4]. B7-H3, a member of the B7 costimulatory molecule family, was initially identified in 2000 [5]. Since its discovery, investigators have focused on its biological functions in tumor immunity [6C8]. Furthermore, many studies also demonstrated that the soluble form of B7-H3 (sB7-H3) was aberrant in malignant tumors Argatroban and correlated with the poor prognosis, and sB7-H3 could be the potential diagnostic and therapeutic target in tumor diseases [9C11]. There are few reports about the correlation between the B7-H3 molecule and autoimmune disease. Until now, few clinical reports demonstrated the role of B7-H3 in autoimmune diseases besides previous studies found altered soluble B7-H3 expression in rheumatoid arthritis and multiple sclerosis disease and correlation with clinical parameters [12, 13]. In the present study, we aimed to evaluate the expression of soluble B7-H3 in the SLE patients and determine whether its expression levels are related to the SLE disease state. These studies could interpret the mechanism of B7-H3 in autoimmune disease and Argatroban assess if B7-H3 could be the therapeutic target in SLE. We collected the peripheral blood of 78 SLE patients and employed ELISA technique to identify the soluble B7-H3 (sB7-H3) expression pattern and further evaluated its correlation with the degree of disease activity, clinical manifestations, laboratory test indicators, and SLE-related inflammatory cytokine levels. 2. Subjects and Methods 2.1. Subjects This study included 78 SLE patients with their peripheral blood collected in the Department of Rheumatology, Suzhou Hospital of Traditional Chinese Medicine, Jiangsu Province, China, from January 2013 Argatroban to July 2015. All patients fulfilled at least four SLE diagnostic criteria published by the American College of Rheumatology. Among those 78 patients, 14 patients of which were newly diagnosed and 9 patients had never received any treatment prior to the blood draw. The other 55 patients received immunosuppressive therapy or hormonal therapy. The disease activity score of SLE was evaluated by the systemic lupus erythematosus disease activity Rabbit Polyclonal to B-RAF index (SLEDAI) score. We divided the SLE patients into two groups (active and inactive phases) Argatroban based on the degree of disease activity as assessed by the scores of SLE disease activity index (SLEDAI). Patients with SLEDAI scores of 6 were classified to be in the active phase. Those with 0C5 SLEDAI scores were classified to be in the inactive phase. The research protocol of this study was approved by the Ethics Committee of Suzhou Vocational Health College. Among the 78 SLE patients, 75 subjects were females, with an average age of 38.7??15.0 years and the average course of the disease of 1 1.46??2.10 years. Peripheral blood of 52 healthy volunteers who had normal physical examinations was collected in May 2015 as control subjects. These healthy volunteers had no history of allergy and autoimmune disease. There were no significant differences of age between the SLE and the healthy control groups (Table 1). The peripheral blood was collected and a centrifugation was followed to obtain serum. Collected serum was stored at ?80C for later analysis. Table 1 Demographic data of SLE patients and healthy control subjects. = 78)= 52)test was used to analyze the data. Nonlinear regression analysis was used to determine the correlation between the clinical examination indices and degree of disease activities as well as the correlation between sB7-H3 expression and inflammatory cytokine levels (IL-6, IFN- 0.05 was considered statistically significant. 3. Results 3.1. SLE Patients.