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Expression data from stimulated or unstimulated human CD4+ T cells incubated with edelfosine

ABSTRACT: The cytotoxic drug edelfosine is a synthetic analog of 2-lysophosphatidylcholine. Edelfosine is incorporated by highly proliferating cells, e.g. activated immune cells. It is unknown if the described mechanisms for edelfosine action attained by in vitro approaches exclusively contribute to the observed EAE-amelioration or if edelfosine may exert additional, probably more general and possibly immunoablative effects within the setting of autoimmunity. We used microarray analysis in order to confirm proposed mechanisms of edelfosine action, but also to discover novel effects of edelfosine in the context of immune cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44392 | GEO | 2014/05/06

SECONDARY ACCESSION(S): PRJNA189743

REPOSITORIES: GEO

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Expression data from stimulated or unstimulated human CD4+ T cells incubated with edelfosine

Project description:The cytotoxic drug edelfosine is a synthetic analog of 2-lysophosphatidylcholine. Edelfosine is incorporated by highly proliferating cells, e.g. activated immune cells. It is unknown if the described mechanisms for edelfosine action attained by in vitro approaches exclusively contribute to the observed EAE-amelioration or if edelfosine may exert additional, probably more general and possibly immunoablative effects within the setting of autoimmunity. We used microarray analysis in order to confirm proposed mechanisms of edelfosine action, but also to discover novel effects of edelfosine in the context of immune cells. For gene-expression analysis enriched CD4+ T cells obtained from Buffy Coats were plated at 200,000 cells/well in 96-well plates. Cells were cultured for 30 h in X-Vivo 15 medium or X-Vivo 15 medium supplemented with 3.3 ug/ml edelfosine, 10 ug/ml edelfosine, bead particles coated with antibodies against CD2, CD3, and CD28 (Miltenyi), or 3.3 ug/ml edelfosine in combination with bead particles coated with antibodies against CD2, CD3 and CD28, respectively.

2014-05-06 | E-GEOD-44392 | biostudies-arrayexpress

EAE_CD3_Sp/Br

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Pregnancy enables expansion of autoreactive regulatory T cells in an animal model of multiple sclerosis

Project description:Disease activity of autoimmune disorders such as multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) is temporarily suppressed by pregnancy. However, whether disease amelioration is due to non-specific immunomodulation or mediated by antigen-specific regulation of disease-causing conventional T cells (Tcon) and immuno- suppressive regulatory T cells (Treg), remains elusive. In the present study, we systematically analyzed changes of the T cell receptor (TCR) β repertoire driven by EAE and pregnancy using TCR sequencing. We demonstrate that EAE, but not pregnancy, robustly increased TCR repertoire clonality in both peripheral Tcon and Treg. Notably, pregnancy was required for the expansion of Treg harboring the dominant EAE-associated TRBV chain 13.2 and increased the frequency of EAE-associated clonotypes within the Treg compartment. Our findings indicate that pregnancy supports the expansion of Treg clonotypes that are equipped to recognize EAE- associated antigens. These Treg are thereby particularly suited to control corresponding encephalitogenic Tcon responses and likely contribute to pregnancy-associated protection in autoimmunity.

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Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

Project description:We aimed to investigate the role of EphB3 and EfnB3 on the regulation of astrocyte and microglial responses in the context of CNS inflammation, we KD Efnb3 in microglia or EphB3 in astrocytes both resulting in a comparable amelioration of EAE. The transcriptional analysis of the two cell types revealed the decreased expression of genes associated to inflammation and neurodegeneration in both KD conditions.

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Identification of LGALS1 binding partners in T84 cells by proteomics using a photocrosslinking GlcNAc analog

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Augmentation of a neuroprotective myeloid state by hematopoietic cell transplantation: Control Cohort

Project description:Multiple sclerosis (MS) is an autoimmune disease associated with inflammatory demyelination in the central nervous system (CNS). Autologous hematopoietic cell transplantation (HCT) is under investigation as a promising therapy for treatment-refractory MS. Here we identify a reactive myeloid state in chronic experimental autoimmune encephalitis (EAE) that is surprisingly associated with neuroprotection and immune suppression. HCT in EAE mice leads to an enhancement of this myeloid state, as well as clinical improvement, reduction of demyelinated lesions, decrease in effector T cells, and amelioration of reactive astrogliosis reflected in reduced expression of EAE-associated gene signatures in oligodendrocytes and astrocytes. Further enhancement of myeloid cell incorporation into the CNS following a modified HCT protocol results in an even more consistent therapeutic effect corroborated by additional amplification of HCT-induced transcriptional changes, hence underlining myeloid-derived beneficial effects in the chronic phase of EAE. Replacement or manipulation of CNS myeloid cells thus represents an intriguing therapeutic direction for inflammatory demyelinating disease.

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Augmentation of a neuroprotective myeloid state by hematopoietic cell transplantation

Project description:Multiple sclerosis (MS) is an autoimmune disease associated with inflammatory demyelination in the central nervous system (CNS). Autologous hematopoietic cell transplantation (HCT) is under investigation as a promising therapy for treatment-refractory MS. Here we show that the enhancement of a reactive myeloid response following HCT is neuroprotective in chronic experimental autoimmune encephalitis (EAE). Myeloid cells are the CNS population with the strongest transcriptional changes in chronic EAE, which are further promoted by HCT. HCT leads to clinical improvement, reduction in demyelinated lesions, and amelioration of reactive astrogliosis reflected in reduced expression of EAE-associated gene signatures in oligodendrocytes and astrocytes. Enhanced incorporation of circulation-derived myeloid cells into the CNS results in a more consistent therapeutic effect corroborated by additional amplification of HCT-induced transcriptional changes, underlining myeloid-derived beneficial effects in the chronic phase of EAE. Replacement or manipulation of CNS myeloid cells thus represents an intriguing therapeutic direction for inflammatory demyelinating disease.

2024-01-04 | GSE217529 | GEO

Effect of Clostridia strains on EAE clinical outcome as a therapeutic treatment

Project description:Researchers have induced an experimental model of multiple sclerosis [experimental autoimmune encephalomyelitis (EAE)] in mice to investigate the therapeutic effect of the oral treatment with selected Clostridia strains on the clinical outcome of EAE and its mechanisms of action

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edelfosine and wortmannin effect at 22°c and 4°c-PI4-kinase and phospholipase C signaling in cold response

Project description:rs09-04_plc_2 - edelfosine and wortmannin effect at 22°c and 4°c - Is there an overlap between PI4-kinase and phospholipase C signaling in cold response ? - Experiments were carried out with Columbia suspension cells. Cells were treated or not with edelfosine (PLC inhibitor) or wortmannin (PI4-kinase inhibitor). These agents were added 15 min before cold stress. ARN were extracted 4h after stress. Controls were made at 22°C. Keywords: treated vs untreated comparison

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