Clinical Reviews in Allergy & Immunology

, Volume 27, Issue 1, pp 23–34

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
Article

DOI: 10.1385/CRIAI:27:1:023

Cite this article as:
Holgate, S.T., Davies, D.E., Rorke, S. et al. Clinic Rev Allerg Immunol (2004) 27: 23. doi:10.1385/CRIAI:27:1:023

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.

Index Entries

Metalloproteinase bronchial hyperreactivity ADAM T helper-2 inflammation 

Copyright information

© Humana Press Inc. 2004

Authors and Affiliations

  • Stephen T. Holgate
    • 1
  • Donna E. Davies
    • 1
  • Steuart Rorke
    • 1
  • Julie Cakebread
    • 1
  • Gillian Murphy
    • 2
  • Robert M. Powell
    • 1
  • John W. Holloway
    • 1
  1. 1.Respiratory Cell & Molecular Biology Research Division, School of MedicineUniversity of SouthamptonUK
  2. 2.Cambridge Institute for Medical ResearchUniversity of CambridgeUK
  3. 3.IIR Division (810), D Level Centre BlockSouthampton General HospitalSouthamptonUK