The significant reduction of macrophage phagocytotic capability in these patients suggests the potential for disease recurrence. The use of a serum-free method confirmed the presence of intrinsic factors that modulate the decrease of macrophage function in SLE.

Background Transglutaminase 2 (TG 2) is a crosslinking enzyme that is known for tissue stabilization and immediate defense against injury or infection in many biological systems. Abnormal TG 2 activity in tissues contributes to a variety of diseases including autoimmune diseases. Objectives The aim of this study was to investigate the mRNA expression of TG 2 on peripheral blood mononuclear cells (PBMCs) in patients with systemic lupus erythematosus (SLE) and in patients with rheumatoid arthritis (RA) and further to determine its association with clinical features. Methods Forty patients with SLE (3 males, 37 females) and thirty two patients with RA (8 males, 24 females) attending outpatient clinics at Taichung Veterans General Hospital were enrolled in this study. Thirty three age-matched healthy subjects from the local community served as controls. About 30 mL blood was collected into sterile tubes containing EDTA. PBMCs were isolated with lymphocyte-separation medium by the density gradient separation. Total RNA was isolated from PBMCs of patients with SLE, patients with RA, and healthy subjects. RNA was extracted by using Trizol reagent and RNA samples were resuspended in diethyl pyrocarbonate-treated water followed by quantification of RNA concentration and purity by a spectrophotometer with calculating the ration of optical density at wavelengths of 260 and 280 nm. The first-strand cDNA for RT-PCR was synthesized from total RNA using the RT-PCR system. The cDNAs encoding human TG 2 and GAPDH were amplified by RT-PCR using the appropriate primer pairs, respectively. Results The mRNA expression of TG 2 in SLE patients was significantly higher than that in RA patients and healthy controls. However, there was no significant difference for mRNA expression of TG 2 between RA patients and healthy controls. In SLE patients with aged 20-50 years, the mRNA expression of TG 2 tended to increase with age but was decreased in elderly SLE patients. In contrast, the mRNA expression of TG 2 tended to decrease with age in RA patients and elderly RA patients had lower mRNA expression of TG 2. In addition, there were correlations of TG 2 mRNA expression with clinical features in both SLE and RA patients. Conclusions The mRNA expression of TG 2 was increased in patients with SLE. Age-related change in mRNA expression of TG 2 was observed in both SLE patients and RA patients. However, the differential mechanism for TG 2 involvement in the pathogeneses of autoimmune diseases including SLE and RA needs further investigation. Disclosure of Interest None Declared

Background Patients with rheumatoid arthritis (RA) tend to have higher incidence of atherosclerosis and the chances of stroke or myocardial infarction also increase significantly in those patients. CD36 is responsible for the major part of oxidized low-density lipoprotein (ox-LDL) uptake by macrophages, suggesting atherogenic properties for CD36. Advanced glycation end products (AGEs) are a heterogeneous group of substances formed by the nonenzymatic glycation in serum and tissues. Matrix metalloproteinases (MMPs) are responsible for the degradation of most extracellular matrix proteins and mediate tissue remodeling in a variety of pathologic conditions. Objectives The aim of this study was to identify CD36 mRNA expression and to determine its association with the circulating levels of AGEs and MMPs in patients with RA. Methods A total of 60 subjects, including thirty patients with RA and thirty healthy subjects participated in this study. Peripheral blood mononuclear cell RNA was used to analyze the CD36 mRNA expression by RT-PCR. Plasma concentrations of the AGEs, ox-LDL, receptor for AGEs (RAGE), interleukin-17 (IL-17), matrix metalloproteinases-2 (MMP-2), MMP-9, tissue inhibitor of metalloproteinases-1 (TIMP-1), and TIMP-2 were determined by enzyme-linked immunosorbent assay. Results CD36 mRNA expression in RA patients was significantly lower than healthy subjects. AGEs and MMP-9 concentrations of RA patients were significantly higher but RAGE levels were significantly lower than those in healthy subjects. RA patients have increased ox-LDL levels along with increased cardiovascular risk. In RA patients, plasma AGEs concentration positively correlated with fasting insulin, TC/HDL-C, and IL-17, whereas ox-LDL concentration positively related to MMP-2 and TC/HDL-C. Conclusions RA patients have reduced CD36 mRNA expression and decreased RAGE along with abnormal levels of AGEs and MMPs, suggesting the risk of atherosclerosis in RA patients may at least in part relate to interaction of glycation, oxidation, and MMP function. Disclosure of Interest None Declared