A novel estrogen receptor 1: sphingomyelin phosphodiesterase acid-like 3B pathway mediates rituximab response in myositis patients
Authors' conclusion
In addition to B-cell depletion, rituximab may be beneficial in myositis due to increased ESR1 signalling mediated by rituximab binding to SMPDL3B on skeletal muscle cells.
Study context
- Population
- Patients from the rituximab in myositis (RIM) trial; immortalized myotubes and primary human DM muscle cells in vitro
- Participants
- 10 RIM trial patients
- Comparison
- Rituximab responders vs non-responders
- Respondersn = 5
- Non-respondersn = 5reference
Methodological detailsmuscle biopsies at baseline and 16 weeks post treatment, in vitro
- Muscle biopsies at baseline and 16 weeks post treatment
- In vitro
Main finding
As reported in the abstract
16 weeks post treatment
- Increased number of changes in gene expression in responders vs non-responders
- Completely different changes in microRNA and mRNA expression in the two groups, except one mRNA, BHMT2
- ESR1 upregulated in responders
- ESR1 upregulation confirmed upon rituximab treatment of immortalized myotubes and primary human DM muscle cells in vitro
- Primary human DM muscle cells did not express CD20 but expressed SMPDL3B
Original publication
A novel estrogen receptor 1: sphingomyelin phosphodiesterase acid-like 3B pathway mediates rituximab response in myositis patients. Rheumatology (Oxford). Published 8 December 2022. doi:10.
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