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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide analysis of lupus immune complex stimulation of peripheral blood mononuclear cells and how this is regulated by C1q

ABSTRACT: The goal of this study was to determine what genes are up- and down-regulated in response to lupus immune complexes in total peripheral blood mononuclear cells (PBMCs). Our results have shown that novel genes are induced by immune complexes that are likely important for lupus pathogenesis plus that C1q regulates these pathways and induces multiple new pathways not previously identified. Total RNA was isolated from PBMCs from 2 donors after 5 hours with the following condiitons: 1) Unstimulated, 2) Lupus immune complex alone, 3) Lupus immune complex + C1q, 4) C1q alone

ORGANISM(S): Homo sapiens

SUBMITTER: Deanna Santer

PROVIDER: E-GEOD-32279 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of lupus immune complex stimulation of purified CD14+ monocytes and how this response is regulated by C1q

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

2011-12-07 | E-GEOD-32278 | biostudies-arrayexpress

Genome-wide analysis of lupus immune complex stimulation and how this response is regulated by C1q

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

2011-12-07 | E-GEOD-32285 | biostudies-arrayexpress

Genome-wide analysis of lupus immune complex stimulation of peripheral blood mononuclear cells and how this is regulated by C1q

Project description:The goal of this study was to determine what genes are up- and down-regulated in response to lupus immune complexes in total peripheral blood mononuclear cells (PBMCs). Our results have shown that novel genes are induced by immune complexes that are likely important for lupus pathogenesis plus that C1q regulates these pathways and induces multiple new pathways not previously identified.

2011-12-07 | GSE32279 | GEO

Genome-wide analysis of lupus immune complex stimulation of purified CD14+ monocytes and how this response is regulated by C1q

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Discovery of Novel Circulating Immune Complexes in Lupus Nephritis Using Immunoproteomics

Project description:The goal is to discover novel circulating immune complexes (ICx) in the serum of Lupus Nephritis (LN) as potential biomarkers. Protein A/G magnetic beads or C1q-coated plates were used to capture ICx in the serum of LN, followed by the identification of immunoglobulin-binding proteins using liquid chromatography and tandem mass spectrometry (LC-MS/MS). Six related genomic-level databases were used for selecting potential biomarkers, following ELISA validation with independent samples.

2022-05-20 | PXD031069 | Pride

Genome-wide analysis of lupus immune complex stimulation and how this response is regulated by C1q

Project description:Genome-wide analysis of lupus immune complex stimulation and how this response is regulated by C1q

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Lupus autoantibodies initiate a maladaptive homeostasis sustained by HMGB1:RAGE signaling and reversed by LAIR-1:C1q signaling

Project description:Cognitive impairment is a frequent manifestation of neuropsychiatric systemic lupus erythematosus (NPSLE), present in up to 80% of patients and leading to a diminished quality of life. We have developed a model of lupus-like cognitive impairment which is initiated when anti-DNA, anti-N-methyl D-aspartate receptor (NMDAR) cross- reactive antibodies, which are present in 30% of SLE patients, penetrate the hippocampus. This leads to immediate, self-limited excitotoxic death of CA1 pyramidal neurons followed by loss of dendritic arborization in the remaining CA1 pyramidal neurons and impaired spatial memory. Both microglia and C1q are required for dendritic loss. Here we show that this pattern of hippocampal injury creates a maladaptive homeostasis that is sustained for at least one year. It requires HMGB1 secretion by neurons to bind RAGE, a receptor for HMGB1 expressed on microglia, and leads to decreased expression of microglial LAIR-1, an inhibitory receptor for C1q. The angiotensin converting enzyme (ACE) inhibitor captopril, which can restore a healthy homeostasis, microglial quiescence, and intact spatial memory, leads to upregulation of LAIR-1. This paradigm highlights HMGB1:RAGE and C1q:LAIR-1 interactions as pivotal pathways in the microglial–neuronal interplay that defines a physiologic versus a maladaptive homeostasis.

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Complement C3 deposition on nucleic acids is characteristic of immune complex initiated classical pathway overdrive in lupus erythematosus

Project description:Systemic lupus erythematosus is progressive, immune complex-mediated autoimmune disease targeting numerous organs. A central feature of the disease is the development of antibodies against nuclear components, including DNA. Antibodies against double-stranded DNA are so characteristic of this disease that their detection constitutes one of the criteria for diagnosis. We examined the formation of immune complexes on the surface of autoantigen microarrays incubated in the sera of 39 inactive and 22 active lupus patients and of 31 control subjects. Three different kinds of nucleic acids, dsDNA, ssDNA and RNA were used as antigens, along with chromatin (nucleosomal extract) and several other reference molecules. The composition with respect to IgG, IgM and complement components C3 and C4 was determined. We find that while IgM and C4 are physiological components of immune complexes formed from nucleic acids, both IgG and C3 are extremely characteristic of lupus patients. Complement C4 deposition changes were not consistent: these increased on ssDNA and RNA, decreased on chromatin and did not change significantly on dsDNA. The presence of IgG and C3 in the immune complexes formed from different nucleic acids was characteristic for both active and inactive lupus patients. Receiver-operating curve statistics indicate that C3 deposition measurements can improve the efficiency of identification of inactive lupus patients. These observations reveal the complexity of immune profile changes accompanying SLE. C3, IgM, C4 and IgG binding in 92 human serum samples were examined using custom-made protein arrays

2012-09-30 | E-GEOD-26768 | biostudies-arrayexpress

Defining the cellular proteolytic landscape in systemic lupus erythematosus

Project description:Mass spectrometry analysis of cellular targets of protein degradation in PBMCs of healthy individuals and systemic lupus

2018-10-11 | PXD009112 | Pride

C1q elicited macrophage gene expression

Project description:We have data from a previous microarray experiment which shows that C1q elicits macrophages to express genes important for clearance of dead (apoptotic) cells. In this experiment we want to determine the signaling mechanism by which C1q is turning on macrophage gene expression. For our control (sample 1-3) we heated C1q to denature it so it is inactive. We also want to know which portion of C1q is responsible for activation the macrophage so we generated C1qtails (samples 4-5). We also have macrophages treated with the whole C1q molecule (7-9). And finally we have a cell line (J774) treated with C1q but does not activate the cells (samples 10-12). Bone marrow derived macrophages or J774 cells were adhered to heat inactivated C1q, C1q tails or C1q for 18 hours. Cells were harvested and RNA was isolated and converted to double stranded cDNA and subsequently labeled and hybridized onto NimbleGen mouse gene expression array [100718_MM9_EXP] using Nimblegen Hybridization system 4 according to manufacturerM-bM-^@M-^Ys instructions (Roche)

2014-07-10 | E-GEOD-48619 | biostudies-arrayexpress

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