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ABHD11 inhibition drives sterol metabolism to modulate T cell effector function and alleviate autoimmunity

Chronic inflammation in autoimmunity is driven by hyperactive T cells with dysregulated metabolism. ABHD11 is a mitochondrial hydrolase that supports alpha-ketoglutarate dehydrogenase function and has been associated with remission in rheumatoid arthritis. To explore its role in T cell function, we used CRISPR/Cas9 to knock down ABHD11 in Jurkat T cells and performed RNA-Seq analysis. Differential gene expression revealed widespread transcriptional changes, with sterol-related pathways among the most significantly enriched. These findings highlight ABHD11 as a potential regulator of metabolic programming in T cells with implications for autoimmunity.

Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data

Dataset ID Description Technology Samples
EGAD50000001845 Illumina NovaSeq 6000 8
Publications Citations
Mitochondrial ABHD11 inhibition drives sterol metabolism to modulate T-cell effector function.
Nat Commun 16: 2025 9484
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