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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease

ABSTRACT: Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease

PROVIDER: PRJNA802547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17846230_1.fastq.gz	Fastqsanger.gz
	SRR17846230_2.fastq.gz	Fastqsanger.gz
	SRR17846231_1.fastq.gz	Fastqsanger.gz
	SRR17846231_2.fastq.gz	Fastqsanger.gz
	SRR17844035_1.fastq.gz	Fastqsanger.gz

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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scRNA-seq)

Project description:Protein arginine methyltransferase 5 (Prmt5) is the major type II methyltransferase catalyzing symmetric dimethylation, regulates cell development, homeostatic and disease processes. Prmt5 inhibition or deletion in CD4+T cells has been reported to protection against experimental autoimmune encephalomyelitis (EAE), the perfect mouse model for multiple sclerosis (MS); however, the detail mechanisms have not yet been elucidated. Here, using the mRNA sequencing, single cell RNA sequencing and ATAC sequencing, we uncovered the unreported role of Prmt5 on T cells migration ability under the EAE condition. We found that mice condition knockout of Prmt5 in T cells were resistance with EAE, infiltrating inflammatory CD4+ T cells in center nervous system (CNS) were greatly reduced. However, T cells in spleen showed much more proliferation and activation properties in Prmt5cko mice, the number of pathogenic CD4+T cells in spleen were not reduced. We further revealed that Rora+CD4+T cells were elevated in Prmt5cko mice, but expressed lower level of S1pr1, resulting in a lack of CD4+ T cells egress from spleen and migrate to CNS, leading to pathogenic CD4+T cells were blocked in spleen. Moreover, single cell ATAC sequencing revealed that Klf2 were enriched in S1pr1 promoter and reduced in Prmt5cko mice. Correctively, our study delineated the undiscovered role of Prmt5 on T cell biology, Prmt5 may through Klf2-S1pr1 pathway and regulate T cells migration; modulating Prmt5 levels may be useful for controlling CD4+T cell migration in CD4+T cell mediated diseases including MS.

2023-08-09 | GSE195887 | GEO

Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scATAC-seq)

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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (RNA-seq)

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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (RNA-seq)

Project description:Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (RNA-seq)

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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scRNA-seq)

Project description:Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scRNA-seq)

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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scATAC-seq)

Project description:Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease (scATAC-seq)

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Prmt5 deficiency inhibits CD4+T cells migration through Klf2-S1pr1 and ameliorates EAE disease

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Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

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Project description:To evaluate the potential of EphB3 as a therapeutic target during CNS inflammation, we induced EAE in B6 WT mice and starting at the peak of the disease we initiated treatment with A38 administered. A38 administration ameliorated EAE, and the transcriptional analysis of the astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration.

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

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

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