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Unconventional role of HMGCS1 in driving pathogenic-Th17 cell immunity and autoimmune diseases

GSE306371 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2026/03/18 Platform GPL28330Platform GPL34290
At a glance

RNA-seq (gene expression) · mouse · 16 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
16 samples: 5 × pTh17_WT vs 5 × pTh17_cKO vs 3 × pTh17_Mock vs 3 × pTh17_HiGroups 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.
Summary (written by the submitters)
Identifying factors controlling pathogenic-Th17 cells is of importance, for their vital role in inflammation and immune-pathology. While intricate ER stress signals have been implicated in T cell biology, its role in Th17 cells remain poorly understood. Here, we demonstrated that HMGCS1, a cholesterol biosynthesis precursor enzyme, was highly induced by inflammatory cytokines and preferentially expressed by pathogenic-Th17 cells in vitro and in vivo.
Read the full summary ↓
HMGCS1 specifically dictated pathogenic-Th17 cell differentiation and augmented autoimmune diseases. Nonetheless, HMGCS1 role in pathogenic-Th17 cells was independently of cholesterol metabolism but necessitated its catalytic Cys129 residue. Notably, HMGCS1 leveraged IRE1a-XBP1s-dependent ER stress response which was essential for pTh17 cell generation and pathogenicity by transcriptionally activating Rorc loci. Mechanistically, HMGCS1 located to the ER membrane, where it bound and stabilized IRE1a protein via restraining IRE1a interaction with K48-linked ubiquitination-dependent E3 ligase MARCH5. Of note, interfering HMGCS1 and ER stress impeded pathogenic-Th17 immunity and mitigated autoimmune diseases. Therefore, our work reveals a non-canonical axis wherein HMGCS1 sustains ER stress to license pTh17 cell differentiation during autoimmune responses.
This dataset
Open GSE306371 in finder → Find more mouse RNA-seq datasets →
Download · which file do I need?

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.

1 · Just have a look

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.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE306371_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

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.

Raw reads on ENA ↗

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 PRJNA1310542 and SRA study SRP612549. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
5 × pTh17_WT vs 5 × pTh17_cKO vs 3 × pTh17_Mock vs 3 × pTh17_Hi

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 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.

Samples in this study
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