Vasculitis & polymyalgia rheumatica
Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica
Authors' conclusion
Neutrophil activation, including NET formation, is increased in PMR, through IC-mediated engagement of FcγRIIA.
Study context
- Population
- Patients with PMR and healthy individuals
- Participants
- 60 vs 30
- Comparison
- PMR vs healthy individuals; PMR at flare vs after GC treatment
- PMRn = 60
- Healthy individualsn = 30reference
- Outcome
- Markers of neutrophil activation (plasma IC, calprotectin, NETs by ELISA)
Main finding
As reported in the abstract
- Immune complexes (ICs) in plasma up-regulated neutrophil activation markers CD66b and CD11b
- P < 0.0001
- Up-regulation FcγRIIA-dependent
- P < 0.01
- Circulating IC correlated with plasma-induced CD66b
- r = 0.51, P = 0.004
- Circulating IC correlated with plasma-induced CD11b
- r = 0.46, P = 0.01
Further findings
Calprotectin after GC therapy
- Calprotectin significantly decreased after GC therapy, in contrast to neutrophil extracellular traps (NETs)
- P < 0.001
Calprotectin, PMR without vs with overlapping GCA
- Higher in PMR without overlapping GCA than with overlapping disease
- P = 0.014
Calprotectin and musculoskeletal involvement · before initiation of GC therapy
- Musculoskeletal involvement associated with elevated calprotectin
- P = 0.036
Original publication
Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica. Rheumatology (Oxford). Published 23 December 2022. doi:10.
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