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Eur J Intern Med. 2010 Jun;21(3):157-63. doi: 10.1016/j.ejim.2010.03.005. Epub 2010 Mar 30.

Targeting IL-1beta in disease; the expanding role of NLRP3 inflammasome.

Author information

1
First Department of Internal Medicine, Democritus University of Thrace, Alexandroupolis, Greece.

Abstract

NLRP3 inflammasome activation and IL-1beta secretion have recently emerged as a central mechanism in the pathogenesis of disease. Genetically defined syndromes like cryopyrin-associated periodic syndromes (CAPS, cryopyrinopathies) and familial Mediterranean fever (FMF) or diseases associated with NLRP3 activation by danger signals like gout, pseudogout, Alzheimer's disease or type 2 diabetes are included in this group of diseases. The contribution of anakinra, a recombinant, nonglycosylated human IL-1 receptor antagonist, in both the identification and treatment of such syndromes was considerable. Recently, rilonacept, a long-acting IL-1 receptor fusion protein, and canakinumab, a fully humanized anti-IL-1beta monoclonal antibody, have been developed, with the intention to further extent IL-1beta inhibition treatment strategies to a broader spectrum of disorders beyond the characterized autoinflammatory syndromes, offering a more favorable administration profile. On the other hand, the developed caspase-1 inhibitors, even though effective in experimental models, were not proven efficient in the treatment of inflammatory diseases.

PMID:
20493414
DOI:
10.1016/j.ejim.2010.03.005
[Indexed for MEDLINE]

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