Highlight
– Acute joint bleeding in severe hemophilia A triggers type-I interferon signaling in neutrophils, promoting systemic release of neutrophil extracellular traps (NETs).
– NETs contribute directly to the pathogenesis and progression of hemophilic arthropathy.
– Therapeutic inhibition of the type-I interferon receptor reduces NET formation and attenuates joint damage in a factor VIII knockout mouse model.
– Targeting neutrophil-dependent interferonopathy represents a promising novel strategy to mitigate chronic joint damage in hemophilia patients.
