Project description:This SuperSeries is composed of the following subset Series: GSE32278: Genome-wide analysis of lupus immune complex stimulation of purified CD14+ monocytes and how this response is regulated by C1q GSE32279: Genome-wide analysis of lupus immune complex stimulation of peripheral blood mononuclear cells and how this is regulated by C1q Refer to individual Series
Project description:Systemic sclerosis (SSc) is an autoimmune disease and several distinct autoantibodies have been described in SSc patients, many correlating with specific clinical presentation. Numerous studies have documented the presence of immune complexes (IC) in sera, lungs and BAL of SSc patients, potentially implicating them in the pathogenesis. Monocyte/macrophage activation also have been observed in fibrotic SSc skin and lung tissue. While the upstream activators remain unknown, it is plausible that IC are amongst the key triggers in activating monocytes and sustaining the chronic inflammation and fibrosis in SSc tissue. To test this hypothesis and find the specific downstream genes regulated by IC, we compare the gene expressions of the monocytes stimulated by control medium, LPS and IC using RNA seq. OPN was one of these IC regulated genes. Our paper further suggested that circulating OPN levels serve as a systemic proxy for IC driven profibrotic macrophage activity, highlighting its potential as a promising biomarker in SSc-ILD.
Project description:The rise of PM2.5 in air pollution correlates with increased disease exacerbation, especially in asthma. This study aims to examine how Chiang-Mai, Thailand PM2.5 (CM-PM2.5) affects innate immune responses in primary human monocytes. A transcriptomic profile was obtained from cells that were stimulated with low and high doses of CM-PM2.5 (5 and 20 μg/ml) for 24 hr. The data indicated that primary human monocytes respond to CM-PM2.5 in a dose-dependent manner. The pyrimidine ribonucleotide metabolism was predominant in both datasets, but the suppression of glycolytic rate was found in high doses of CM-PM2.5 stimulation. The upregulation of the key metabolic genes was unable to compensate for the suppression. Moreover, CM-PM2.5 priming induced immune tolerance during subsequent LPS stimulation in primary human monocytes from asthma.
Project description:The goal of this study was to determine what genes are up- and down-regulated in response to lupus immune complexes in purified CD14+ monocyte stimulations. Our results have shown that novel genes are induced by immune complexes but the response is less robust when using purified monocytes versus total PBMCs Total RNA was isolated from CD14+ monocytes from 2 donors after 5 hours with the following conditions: 1) Unstimulated, 2) Lupus immune complex alone, 3) Lupus immune complex + C1q, 4) C1q alone
Project description:Slan+ Non-Classical Monocytes migrate on immobilized immune complexes. This phenomenon can be blcoked with anti-CD16 blocking antibodies and is therefore thought to be mediated via CD16 (FcyRIII). Nonetheless, other CD16+ cells, such as NK cells or neutrophils, as well as lineage related cells suchs as classical monocytes do not migrate on immobilized immune complexes. We therefore isolated protein content of Slan+ Non-Classical Monocytes after migration immobilized immune complexes to perform phosphoproteomics in order to better understand the underlying signaling pathways inducing the migratory response.
Project description:To evaluate gene expression in human peripheral blood derived monocytes over the course of an LPS stimulation time-series. Keywords: time course
Project description:We wished to investigate differential effects of stimulation with immune complex on colonic macrophages taken from mice which were either healthy or had DSS induced colitis.
Project description:As innate immune cells, monocytes play a central role in antifungal immunity. Using proteome studies in primary human monocytes, which were stimulated by Candida albicans (yeast) in vitro. Here we describe the changes of proteins in monocytes and demonstrate that in the early stage of infection, the differences of innate immune response triggered by C. albicans over time.