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The discovery and role of ADAM33, a new candidate gene for asthma

Published online by Cambridge University Press:  23 September 2004

John W. Holloway ,
Tim P. Keith ,
Donna E. Davies ,
Robert Powell ,
Hans-Michael Haitchi  and
Stephen T. Holgate
John W. Holloway
Affiliation:
Human Genetics Division, School of Medicine, University of Southampton, Southampton General Hospital, Southampton, SO16 6YD, UK.
Tim P. Keith
Affiliation:
Department of Human Genetics, Genome Therapeutics Corporation, Waltham, MA 02453, USA.
Donna E. Davies
Affiliation:
Allergy and Inflammation Research, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, D level Centre Block (MP810), Southampton General Hospital, Southampton, SO16 6YD, UK.
Robert Powell
Affiliation:
Allergy and Inflammation Research, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, D level Centre Block (MP810), Southampton General Hospital, Southampton, SO16 6YD, UK.
Hans-Michael Haitchi
Affiliation:
Allergy and Inflammation Research, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, D level Centre Block (MP810), Southampton General Hospital, Southampton, SO16 6YD, UK.
Stephen T. Holgate
Affiliation:
Allergy and Inflammation Research, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, D level Centre Block (MP810), Southampton General Hospital, Southampton, SO16 6YD, UK.
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Abstract

Asthma is a complex disorder in which major genetic and environmental factors interact to initiate the disease and propagate it as a chronic relapsing disorder. Until recently, genetic factors implicated in the disease pathogenesis have been restricted to variants in known molecules involved in the inflammatory or remodelling pathways. This review discusses evidence for a new susceptibility gene for asthma, ADAM33, which was identified by positional cloning and shown to be selectively expressed in mesenchymal but not immune or inflammatory cells. ADAM33 belongs to a family of membrane–anchored metalloproteinases that also have fusagenic, adhesion and intracellular signalling properties. ADAM33 might play a key role in predisposing to the reduced lung function characteristic of asthma, possibly by influencing airway wall remodelling.

Keywords

AsthmaA Disintegrin and Metalloprotease 33GeneticsEpithelial–Mesenchymal Trophic UnitSheddase
Type
Review Article
Information
Expert Reviews in Molecular Medicine , Volume 6 , Issue 17 , 4 August 2004 , pp. 1 - 12
Copyright
© Cambridge University Press 2004

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