Dysregulation of YTHDF2 promotes the over expression of interferon beta in anti-MDA5 antibody-positive dermatomyositis
Authors' conclusion
Our findings suggest a decrease in YTHDF2 expression in anti-MDA5+DM monocytes, potentially enhancing IFNB expression and promoting the activation of JAK-STAT signaling pathway.
Study context
- Population
- Peripheral blood mononuclear cells (PBMCs) and monocytes from anti-MDA5+dermatomyositis (DM) patients and healthy controls (HC); THP-1 cells
- Comparison
- Anti-MDA5+ DM patients vs HC; siYTHDF2-THP-1 cells
Main finding
As reported in the abstract
- Overall mRNA m6A methylation decreased in PBMCs of anti-MDA5+ DM vs HC
- YTHDF2 expression downregulated in PBMCs and monocytes of anti-MDA5+DM vs HC
- IFNB expression increased in PBMCs and monocytes of anti-MDA5+DM
- YTHDF2 knockdown in THP-1 cells significantly increased IFNB expression and activated JAK-STAT signalling
- Interaction between YTHDF2 protein and IFNB mRNA confirmed by RNA immunoprecipitation and quantitative PCR (RIP-qPCR)
- Upregulated type I IFN after YTHDF2 knockdown inhibited by JAKi
Original publication
Dysregulation of YTHDF2 promotes the over expression of interferon beta in anti-MDA5 antibody-positive dermatomyositis. Arthritis Res Ther. Published 24 January 2026. doi:10.
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