ADAM 33 and its association with airway remodeling and hyperresponsiveness in asthma.

Stephen T Holgate, Donna E Davies, Steuart Rorke, Julie Cakebread, Gillian Murphy, Robert M Powell, John W Holloway

Journal: Clinical reviews in allergy & immunology 2005;27(1):23-34

PMID: 15347848

Abstract

Asthma is known to be a Th2 inflammatory syndrome that leads to intermittent airway obstruction. However, the mechanisms involved in development of the clinical features remain enigmatic, although genetic elements clearly are involved. Recently, based on a large genome wide screen involving families in the United Kingdom and the United States with at least two siblings with asthma, a locus was identified that encoded for a family of proteases. This group of proteins is now known as the ADAM superfamily. In this review, we discuss the ADAM superfamily and, in particular, ADAM 33, a member of a family of genes which encode a subgroup of zinc dependent metalloproteinase (metzincin). The potential for therapeutic intervention with ADAM 33 is extremely attractive and further work will not only focus on the specific domains of ADAM 33, but also the mechanisms by which they lead to bronchial hyperreactivity.

Address: Respiratory Cell and Molecular Biology Research Division, School of Medicine, University of Southampton, UK, University of Cambridge, UK. [email protected]
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