Interleukin-1–receptor antagonist in the Muckle–Wells syndrome
PN Hawkins, HJ Lachmann… - New England Journal of …, 2003 - Mass Medical Soc
PN Hawkins, HJ Lachmann, MF McDermott
New England Journal of Medicine, 2003•Mass Medical SocTo the Editor: Studies of hereditary inflammatory disorders have identified novel genes and
pathways that may be involved in inflammation and apoptosis generally. Mutations in one
such gene, variously named NALP3, CIAS1, and PYPAF1, were recently identified as the
cause of the Muckle–Wells syndrome and the familial cold autoinflammatory syndrome1 and
have lately also been associated with neonatal-onset multisystem inflammatory disease. 2
Interleukin-1 is a key proinflammatory cytokine that contributes to increased synthesis of …
pathways that may be involved in inflammation and apoptosis generally. Mutations in one
such gene, variously named NALP3, CIAS1, and PYPAF1, were recently identified as the
cause of the Muckle–Wells syndrome and the familial cold autoinflammatory syndrome1 and
have lately also been associated with neonatal-onset multisystem inflammatory disease. 2
Interleukin-1 is a key proinflammatory cytokine that contributes to increased synthesis of …
To the Editor: Studies of hereditary inflammatory disorders have identified novel genes and pathways that may be involved in inflammation and apoptosis generally. Mutations in one such gene, variously named NALP3, CIAS1, and PYPAF1, were recently identified as the cause of the Muckle–Wells syndrome and the familial cold autoinflammatory syndrome1 and have lately also been associated with neonatal-onset multisystem inflammatory disease.2 Interleukin-1 is a key proinflammatory cytokine that contributes to increased synthesis of serum amyloid A protein by hepatocytes during the acute-phase response. The availability of a recombinant interleukin-1–receptor antagonist for clinical use enabled us to undertake a trial of . . .
The New England Journal Of Medicine