Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32279 | GEO | 2011/12/07

SECONDARY ACCESSION(S): PRJNA154515

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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. 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

2011-12-07 | E-GEOD-32279 | biostudies-arrayexpress

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 purified CD14+ monocytes and how this response is regulated by C1q

2011-12-07 | GSE32278 | GEO

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.

2023-05-01 | GSE230077 | GEO

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

| PRJNA146355 | ENA

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

Microglial-derived C1q integrates into neuronal ribonucleoprotein complexes and impacts protein homeostasis in the aging brain

Project description:Neuroimmune interactions mediate intercellular communication and underlie critical brain functions. Microglia, CNS-resident macrophages, modulate the brain through direct physical interactions and the secretion of molecules. One such secreted factor, the complement protein C1q, contributes to complement-mediated synapse elimination in development and disease models, yet brain C1q protein levels increase significantly throughout aging. How age-related C1q affects neuronal function has not been demonstrated. Here we report that C1q interacts with neuronal ribonucleoprotein (RNP) complexes in an age-dependent manner. Purified C1q protein undergoes RNA-dependent liquid-liquid phase separation (LLPS) in vitro, and the interaction of C1q with neuronal RNP complexes in vivo is dependent on RNA and endocytosis. Mice lacking C1q have age-specific alterations in neuronal protein synthesis in vivo and impaired fear memory extinction. Together, our findings reveal a biophysical property of C1q that underlies RNA- and age-dependent neuronal interactions and demonstrate a unique role of C1q in critical intracellular neuronal processes.

2024-07-01 | PXD052189 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data