Gut-derived metabolites drive Th17 cell pathogenicity in Multiple Sclerosis
RNA-seq (gene expression) · mouse · 10 samples
- What it is
- RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
- Organism
- Mus musculus (mouse)
- Samples
- 10 samples: 5 × Experiment_2_antibiotics vs 3 × Experiment_2_controlGroups are read from the sample names, not from the paper. Check the list below.
- Data you can get
- A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
- Paper
- Gut-derived metabolites drive Th17 cell pathogenicity in multiple sclerosisCell reports · 2025
Read the full summary ↓
Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.
Processed table
The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE282316_RAW.tar (it can run to tens of gigabytes).
Raw sequencing reads
The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.
What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.
Also filed as BioProject PRJNA1188120 and SRA study SRP546218. Searching any of these in the dataset finder brings you back here.
Supports a between-group comparison across 8 samples.
How we read this: 2 replicated groups read from 10 sample titles; they account for 8 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.
- GSM8641246 Experiment_1_control1
- GSM8641247 Experiment_2_control1 Experiment_2_control
- GSM8641248 Experiment_2_control2 Experiment_2_control
- GSM8641249 Experiment_2_control3 Experiment_2_control
- GSM8641250 Experiment_1_antibiotics1
- GSM8641251 Experiment_2_antibiotics1 Experiment_2_antibiotics
- GSM8641252 Experiment_2_antibiotics2 Experiment_2_antibiotics
- GSM8641253 Experiment_2_antibiotics3 Experiment_2_antibiotics
- GSM8641254 Experiment_2_antibiotics4 Experiment_2_antibiotics
- GSM8641255 Experiment_2_antibiotics5 Experiment_2_antibiotics
- GSE298131 Gut microbe-derived metabolites drive psoriatic inflammation via modulation of skin Th17 cells 18 samples shares th17, metabolites, drive
- GSE248106 Roquin-deficient T cells drive pancreatitis and tumorigenesis through IL-17 and Th17-inappropriate Cytokine production 21 samples shares th17, drive
- GSE298306 Immune-responsive gene-1: The mitochondrial Key to Th17 Cell Pathogenicity in CNS Autoimmunity 18 samples shares th17, pathogenicity
- GSE296201 A20’s Linear Ubiquitin Binding Motif Restrains Pathogenic Activation of TH17/22 cells and IL-22 Driven Enteritis [RNA-Seq] 18 samples shares th17, drive
- GSE262540 Myelin oligodendrocyte glycoprotein reactive Th17 cells drive Janus Kinase 1 dependent transcriptional reprogramming in astrocytes and alter cell surface cytokine receptor profiles during experimental autoimmune encephalomyelitis. 12 samples shares th17, drive
- GSE240205 A human STAT3 gain of function variant drives Th17 expansion and IL-22 dependent skin inflammation in a model of psoriasiform dermatitis 24 samples shares th17, drive
- GSE284714 AMPK signaling downstream of adenosine 2A receptor represses Th17 cell pathogenicity through epigenetic and metabolic reprogramming. 15 samples shares th17, pathogenicity
- GSE296200 A20’s Linear Ubiquitin Binding Motif Restrains Pathogenic Activation of TH17/22 cells and IL-22 Driven Enteritis [ATAC-seq] 11 samples shares th17, drive
Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.