CSF B cells in relapsing multiple sclerosis are driven towards an antigen-experienced, inflammatory fate
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA549712 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12483500_1.fastq.gz | Fastqsanger.gz | |||
| SRR12483500_2.fastq.gz | Fastqsanger.gz | |||
| SRR12483501_1.fastq.gz | Fastqsanger.gz | |||
| SRR12483501_2.fastq.gz | Fastqsanger.gz | |||
| SRR12483502_1.fastq.gz | Fastqsanger.gz |
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Project description:This study provides an overview of the transcriptional signature of oligodendrocyte progenitor cells (OPCs) exposed to the CSF collected from multiple sclerosis patients with either a relapsing remitting disease course (RRMS) or a confirmed primary progressive diagnosis (PPMS). Using an Affymetrix microarray we were able to detect a set of common and unique genes for each treatment group. Gene ontology analysis revealed a common group of genes involved in protein transport, actin dynamics and response to stress and DNA damage, while the RRMS-specific genes were grouped according to protein complex biogenesis, nuclear transport and RNA processing. The transcriptional signature of progenitors exposed to PPMS was characterized by an up-regulation of the pro-differentiation adhesion molecule Lgals3. We confirmed increased protein levels of its gene product,product; galectin-3 in proliferating OPCs incubated with CSF from PPMS patients and also found a four-fold increase in mRNA transcript levels of galectin-3 in human post-mortem normal-appearing white matter samples of primary progressive MS patients when compared to non-neurological controls. This study will help to better understand the common and specific transcriptional changes induced in the different subtypes of MS and therefore find more specific molecular targets for each disease subtype.
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