Transcriptional derepression of CHD4/NuRD-regulated genes in the muscle of patients with dermatomyositis and anti-Mi2 autoantibodies
Authors' conclusion
Based on these findings, we hypothesise that anti-Mi2 autoantibodies could exert a pathogenic effect by entering damaged myofibres, inhibiting the CHD4/NuRD complex, and subsequently derepressing the unique set of genes defined in this study.
Study context
- Population
- Muscle biopsies from patients with myositis (dermatomyositis (DM) with and without anti-Mi2, antisynthetase syndrome (AS), immune-mediated necrotising myopathy (IMNM), inclusion body myositis (IBM)) and normal musclemuscle biopsies from patients
- Participants
- 171 biopsies
- Comparison
- Anti-Mi2-positive DM muscle vs other myositis subtypes and normal muscle
- Anti-Mi2-positive DMn = 18
- DM without anti-Mi2n = 32
- ASn = 18
- IMNMn = 54
- IBMn = 16
- Normal musclen = 33reference
- Outcome
- Transcriptional profile of muscle biopsies from anti-Mi2-positive DM patients
Methodological detailsRNA sequencing, immunohistochemistry
- RNA sequencing
- Immunohistochemistry
Main finding
As reported in the abstract
- Genes specifically overexpressed in anti-Mi2-positive DM muscle, incl. SCRT1 and MADCAM1
- 135
Original publication
Transcriptional derepression of CHD4/NuRD-regulated genes in the muscle of patients with dermatomyositis and anti-Mi2 autoantibodies. Ann Rheum Dis. Published 2 May 2023. doi:10.
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