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ABSTRACT: Intestinal microbiome of HOXA11os knock in (HOXA11os-KI) mice and their WT littermate controls

PROVIDER: PRJNA854590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19908102_1.fastq.gz	Fastqsanger.gz
	SRR19908102_2.fastq.gz	Fastqsanger.gz
	SRR19908079_1.fastq.gz	Fastqsanger.gz
	SRR19908079_2.fastq.gz	Fastqsanger.gz
	SRR19908081_1.fastq.gz	Fastqsanger.gz

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Project description:MicroRNAs are small non-coding RNA molecules that fine-tune diverse biological processes and are often found to be dysregulated in diseases, such as multiple sclerosis (MS). MS is an immune-mediated disease of the central nervous system characterized by demyelination, axonal loss and neurodegeneration. We have previously shown microRNA-150 (miR-150) levels to be elevated in cell-free cerebrospinal fluid (CSF) of MS patients compared to controls. We aimed to investigate the physiopathological function of miR-150 in vivo by generating miR-150 knock-out (KO) and knock-in (KI) mice using CRISPR/Cas9 technology. To specifically interrogate the role of miR-150 upon inflammation of the central nervous system (CNS), we induced experimental autoimmune encephalomyelitis (EAE), a mouse model for MS, in these newly generated mice. After induction of EAE, miR-150KO mice developed milder disease compared to WT littermate controls while miR-150KI mice presented with exacerbated EAE. Disease amelioration in miR-150KO was accompanied by decreased infiltration of CD4+ T cells in the central nervous system compared to WT and KI mice, as well as increased FoxP3+ regulatory T (Treg) cells in inguinal lymph nodes at disease priming stage. We demonstrated that Treg cells were fundamental for EAE amelioration in miR-150KO mice, as their partial depletion during EAE priming stage in miR-150KO FoxP3DTR mice restored disease incidence and severity to the levels observed in WT and KI mice. Transcriptomic profiling of CD4+ T cells isolated from miR-150KO mice revealed upregulation of genes associated with Treg cell function, but also reduced gene translation and autophagy, as compared to WT and particularly KI cells. The role of miR-150 in affecting the fate of CD4+ T cells was further supported by the grater tendency of miR-150KO CD4+ T cells to differentiate into Treg cells in-vitro. In conclusion, miR-150 deficiency favored considerably milder CNS inflammation by promoting differentiation of a more anti-inflammatory CD4+ T cell repertoire.

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