Project description:Systemic lupus erythematosus (SLE), also known simply as lupus, is an autoimmune disease. There is no cure for SLE. The mechanism involves an immune response by autoantibodies against a person's own tissues. However, the mechanism underlying imbalance of autoantibodies is not clear. In this experiment, peripheral blood was obtained from normal healthy donors and systemic lupus erythematosus (SLE) patients. Peripheral blood mononuclear cells (PBMC) were separated by Ficoll separation solution. Samples of four (total eight) donors were pooled and Samples of four (total eight) SLE patients were pooled. The aim was to characterize the mRNA profile of SLE patients compared to healthy donors and find the new target of diagnosis or treatment for SLE.
Project description:RNA-seq of systemic lupus erythematosus (SLE) whole blood and healthy controls to determine the gene expression changes in these patients. RNA-seq of PAXgene blood from SLE and healthy donors.
Project description:In this experiment, the miRNA profile of microvesicles (MV) released from activated or apoptotic (UV-B treated) T-lymphocytes and their cells of origin was analyzed in both samples obtained from normal healthy donors and systemic lupus erythematosus (SLE) patients. Therefore in short, RNA was isolated of activated and apoptotic (UV-B treated) T-Lymphocytes and corresponding MV of normal healthy individuals and systemic lupus erythematosus (SLE) patients. Samples of four donors each were pooled. The aim was to characterize the miRNA profile of MV dependent on different release stimuli and compare their miRNA-profile to their cells of origin.
Project description:B cells orchestrate the autoimmune responses in patients with systemic lupus erythematosus (SLE), but broad based B-cell directed therapies only show modest efficacy while attenuating humoral immune responses to vaccines and inducing acquired immunodeficiency. used proteomic and transcriptomic analyses of B cells from patients with SLE and healthy individuals and demonstrated a dominant DDR in SLE B cells.
