Interleukin-6 trans-signalling regulates monocyte chemoattractant protein-1 production in immune-mediated necrotizing myopathy
Authors' conclusion
IL-6 trans-signalling may contribute to the immunopathogenesis of IMNM by augmenting inflammation through regulation of MCP-1 expression in IMNM.
Study context
- Population
- Patients with immune-mediated necrotizing myopathy (IMNM) and controls; human myoblasts in vitro
- Comparison
- IMNM patients vs controls; IL-6/sIL-6R stimulation of human myoblasts
- Outcome
- MCP-1 expression and IL-6 signalling in IMNM
Main finding
As reported in the abstract
- MCP-1 scattered and positively expressed within myofibres and a few inflammatory cells in IMNM muscle
- Sarcoplasmic MCP-1 expression significantly correlated with myonecrosis, myoregeneration and inflammatory infiltration
- Serum MCP-1, IL-6 and sIL-6R elevated in IMNM vs controls
- Serum MCP-1 significantly associated with serum IL-6 and clinical disease severity in IMNM
- IL-6/sIL-6R complex induced MCP-1 expression via the STAT3 pathway in human myoblasts
- Phospho-STAT3 enriched in the MCP-1 promoter region and promoted transcription
Original publication
Interleukin-6 trans-signalling regulates monocyte chemoattractant protein-1 production in immune-mediated necrotizing myopathy. Rheumatology (Oxford). Published 23 February 2024. doi:10.
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