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Microarray Sequencing Analysis of microglia from Wild Type and AIM2-/- mice with EAE

ABSTRACT: We identified that AIM2 protected against MOG-induced EAE, and AIM2 deficiency in microglia promoted the development of EAE. The purpose of this experiment was to identify how AIM2 protected against MOG-induced EAE.

ORGANISM(S): Mus musculus

PROVIDER: GSE151636 | GEO | 2020/06/03

REPOSITORIES: GEO

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Gene expression profiling of mouse experimental autoimmune encephalomyelitis (EAE) from spinal cord preparations of opticospinal EAE (OSE) and MOG-induced EAE

Project description:Genetic opticospinal EAE (OSE) and MOG-induced EAE (MOG-EAE) are two experimental autoimmune encephalomyelitis (EAE) mouse models of human multiple sclerosis. For the OSE model, double-transgenic 2D2 (TCRMOG) x IgHMOG mice were used. For MOG-EAE, wildtype C57BL/6 mice were immunized with a MOG peptide consisting of the amino acids 35-55, administered in complete Freund’s adjuvant containing 5mg / ml Mycobacterium tuberculosi. The severity of EAE was rated on the scale 0: healthy animal; 1: animal with a flaccid tail; [...]; 4: animal with both hind legs paralyzed. The case groups in the experiment were: OSE1: OSE with disease score 1; OSE4: OSE with disease score 4; MOG4: MOG-EAE injected with both MOG and adjuvant, with disease score 4. The control groups in the experiment were: OSE0: OSE with disease score 0; CFA: C57BL/6 mice injected only with adjuvant (no MOG); WT: Wildtype C57BL/6 mice. The aim of the experiment was to assess gene expression differences 1) between OSE4 and OSE0, 2) between OSE1 and OSE0, and 3) between MOG4 and CFA. For control, WT was compared to OSE0 and CFA. Subsequently, differentially expressed transcripts were compared, first, between the OSE4 vs. OSE0 and the MOG4 vs. CFA contrasts (different EAE models) and, second, between the OSE4 vs. OSE0 and the OSE1 vs. OSE0 contrasts (different EAE severity).

2020-08-21 | E-MTAB-9132 | biostudies-arrayexpress

AIM2 in regulatory T (Treg) cells restrains autoimmune diseases

Project description:The inflammasome initiates innate defense and inflammatory response by activating caspase-1 and pyroptotic cell death in myeloid cells1,2. It is comprised of an innate immune receptor/effector, pro-caspase-1 and a common adaptor molecule, ASC (apoptotic speck-containing protein with a CARD). Consistent with their pro-inflammatory function, inflammasome components including caspase-1, ASC and NLRP3, are known to exacerbate autoimmunity during experimental autoimmune encephalomyelitis (EAE) by enhancing IL-1 and IL-18 secretion in myeloid cells3-6. Here we show an unexpected function of a DNA-binding inflammasome effector, AIM2 (Absent in Melanoma 2)7-10, in restraining autoimmunity by performing EAE in both whole body and Treg-specific deletion of Aim2–/– mice. AIM2 is highly expressed by human and mouse Treg cells and it is essential to attenuate EAE. RNA-seq, biochemical and metabolic analyses revealed that AIM2 attenuates mTOR, Myc and immune-metabolic functions in both Treg cells isolated in vivo and Treg cells induced in vitro with TGF-. Importantly, we found AIM2 physically interacted with RACK1 in Treg cells to facility the PP2A/RACK1/Akt-mTOR signaling, which is identified as a central component downstream of AIM2 that controls Treg cell function and stability. While AIM2 is generally accepted as an inflammasome effector in myeloid cells, this report reveals a previously unappreciated T cell-intrinsic role of AIM2 in maintaining Treg cell function to restrain autoimmunity. This is achieved by diminishing Akt-mTOR signaling to regulate Treg stability under inflammation, and altering immune-metabolism in Treg cells.

2021-01-27 | PXD018638 | Pride

Treatment with nanoliposomes loaded with ITE and MOG(35-55) ameliorates EAE

Project description:To evaluate the therapeutic potential of NLP(ITE+MOG) in a mouse model of secondary progressive multiple sclerosis, we induced EAE in NOD mice and initiated weekly treatment with nanoliposomes beginning at 35 days post immunization during the chronic phase of disease. NLP(ITE+MOG) administration ameliorated EAE, and the transcriptional analysis of CNS-resident astrocytes, microglia and monocytes revealed decreased expression of genes associated with pro-inflammatory responses and neurodegeneration.

2021-08-04 | GSE155711 | GEO

Microarray Sequencing Analysis of microglia from Wild Type and AIM2-/- mice with EAE

Project description:Microarray Sequencing Analysis of microglia from Wild Type and AIM2-/- mice with EAE

| PRJNA636743 | ENA

Comparative genomic hybridization of experimental autoimmune encephalomyelitis (EAE)-susceptible DA and EAE-resistant PVG rat strains stimulated with myelin oligodendrocyte glycoprotein (MOG) to identify the alternative splicing.

Project description:Experimental autoimmune encephalomyelitis (EAE)-susceptible DA and EAE-resistant PVG rats were immunized with myelin oligodendrocyte glycoprotein (MOG) to induce an autoimmune response.<br>Seven days later draining inguinal lymph nodes were removed. 2 conditions were examined: 'ex vivo' and 'MOG restimulated', which involved 24hrs of incubation with an encephalogenic MOG 91-108 peptide.

2009-11-01 | E-MEXP-2237 | biostudies-arrayexpress

MOG-encoding DNA vaccines ameliorate EAE and display neuroprotective effects in treated mice summary

Project description:Vaccination with naked DNA encoding myelin basic protein represents a promising therapeutic strategy in multiple sclerosis (MS). In this study, we assessed the potential of vaccination with a DNA construct coding for the myelin oligodendrocyte glycoprotein (MOG), an important candidate autoantigen in MS, to induce tolerance and protect against experimental autoimmune encephalomyelitis (EAE). Herein, we demonstrated that MOG-DNA vaccination reduced the clinical and histopathological signs of EAE when administered in both prophylactic and therapeutic settings. Further mechanistic experiments revealed that the protective effects of MOG-DNA vaccines were associated with a reduction of antigen-specific Th1 and Th17 cellular immune responses and expansion of regulatory T cells in periphery, and up-regulation in the central nervous system of genes encoding neurotrophic factors and proteins involved in remyelination. These results may set the rationale for the use of MOG-based DNA vaccines to induce tolerance in MS patients. We analyzed brain and spinal cord samples from five treated and five control mice

2011-07-08 | E-GEOD-30482 | biostudies-arrayexpress

Microglia and infiltrating monocytes gene expression profiling during EAE progress

Project description:The project was designed to figure out the role of microglia in brain inflammation (EAE model). The first step was to find genes/pathways that are upregulated in the microglia during EAE progress but absent in the infiltrating monocytes. These genes/pathways may provide clues for studying the unique function of microglia in the brain inflammation that is disctinct from the infiltrating monocytes.

2019-12-05 | GSE133180 | GEO

RIPK1 kinase-dependent gene expression in mouse microglia and astrocytes in vivo during EAE

Project description:To determine the role of RIPK1 kinase signaling in microglia and astrocytes during EAE (mouse model of MS), we extracted spinal cords of naive, EAE-vehicle and EAE mice treated with RIPK1 kinase inhibitor (GSK’547) for transcript profiling using RNAseq. We identify various genes that are differentially expressed in EAE disease compared to naive mice, and a subset of these are modulated in a RIPK1 kinase-dependent manner in both astrocytes and microglia. The top RIPK1 kinase-dependent gene pathways include oxidative phosphorylation and mitochondrial dysfunction in microglia and EIF2 signaling and cholesterol biosynthesis in astrocytes. This study demonstractes critical and distinct roles for RIPK1 kinase signaling in both microglia and astrocytes during EAE

2021-08-12 | GSE154228 | GEO

Transcriptome profiling of a backcross between experimental autoimmune encephalomyelitis (EAE)-susceptible DA and EAE-resistant PVG rat strains to identify expression quantitative trait loci.

Project description:The aim of the experiment is to characterize the genetics and mechanisms of the inflammatory response after induction of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, by studying the genome wide expression in the spleen in late disease. A backcross was created between EAE-susceptible DA and EAE-resistant PVG rats. At day 35 after induction of EAE with myelin oligodendrocyte glycoprotein (MOG) in these rats, spleens were taken for transcriptional profiling.

2013-08-10 | E-MTAB-784 | biostudies-arrayexpress

MOG-encoding DNA vaccines ameliorate EAE and display neuroprotective effects in treated mice summary

2011-07-08 | GSE30482 | GEO

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