Omics · study · 2026
The transcription factor Helios is critical for T regulatory cell effector differentiation in organ-specific autoimmunity
Listed in NCBI GEO
The selective deletion of the transcription factor Helios in regulatory T cells (Tregs) leads to systemic immune activation characterized by a Th1 phenotype, hypergammaglobulinemia, and enhanced germinal center formation.
Description
We report here that these mice also exhibit acquired lipodystrophy, hepatic steatosis, and insulin resistance. A significant lymphocytic infiltrate in white adipose tissue indicated autoimmune-mediated destruction of the adipose tissue which was mediated by CD8+ T cells.
In adipose tissue, Helios-deficient Tregs expressed lower levels of Tcf1/Lef1 and thus, exhibited increased effector Tregs (eTregs). However, Helios-deficient Tregs failed to generate functional terminally differentiated eTregs, including ST2+ and CXCR3+ Tregs. Helios bound to regulatory elements in multiple genes known to restrict effector generation, namely Tcf7, Lef1, Bach2, and Id3.
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Thus, Helios restricts eTreg generation but also enforces functional eTreg differentiation. The absence of Helios in Tregs alters eTreg generation and adipose tissue homeostasis and results in the expansion and activation of CD8+ T cells, the destruction of adipose tissue and metabolic disease.
Links
Get the data
- GEO FTP directory ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330646 ↗
download · from NCBI GEO
Where it is published
- GEO accession page ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE330646 ↗
landing page · from NCBI GEO
Documentation and papers
- PRJNA1464792 ncbi.nlm.nih.gov/bioproject/PRJNA1464792 ↗
project · from NCBI GEO
Topics
- Stated by source
- Expression profiling by high throughput sequencing · Mus musculus
- From keywords
- Life Sciences
- Inferred from text
- Disease 75%
Provenance · 1 source records, 8 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| NCBI GEO | GSE330646 | 14 d ago | JSON v1 |
| Field | Assertion | Extractor | Evidence |
|---|---|---|---|
| access_level | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[disease].local:disease:disease | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[field].local:field:life-sciences | mapping · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencing | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /gdstype |
| concepts[organism].NCBITaxon:10090 | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /taxon |
| description | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /summary |
| publication_date | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| title | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /title |