Epithelial IgG and its relationship to the loss of F508 in the common mutant form of the cystic fibrosis transmembrane conductance regulator

Treharne, Kate J.; Cassidy, Diane; Goddard, Catharine; Colledge, William H.; Cassidy, Andrew; Mehta, Anil

doi:10.1016/j.febslet.2009.07.002

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Volume 583, Issue 15 , Pages 2493-2499, 6 August 2009

Epithelial IgG and its relationship to the loss of F508 in the common mutant form of the cystic fibrosis transmembrane conductance regulator

Edited by Gianni Cesareni

Kate J. Treharne
- Division of Medical Sciences, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK
Diane Cassidy
- Division of Medical Sciences, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK
Catharine Goddard
- Physiology, Development and Neuroscience Department, University of Cambridge, Cambridge, UK
William H. Colledge
- Physiology, Development and Neuroscience Department, University of Cambridge, Cambridge, UK
Andrew Cassidy
- DNA Analysis Facility, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK
Anil Mehta
- Division of Medical Sciences, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK
- Corresponding author. Fax: +44 (0)1382 632597.

Received 13 May 2009; received in revised form 22 June 2009; accepted 1 July 2009. published online 09 July 2009.

Abstract

The most debilitating feature of cystic fibrosis (CF) disease is uncontrolled inflammation of respiratory epithelium. The relationship between the commonest mutated form of CFTR (F508del or ΔF508) and inflammation has not yet been elucidated. Here, we present a new paradigm suggesting that CFTR can interact with intra-epithelial IgG, establishing a direct link between normal CFTR and the immune system. Further, our data show that the amino-acid sequence local to F508 can bind IgG with high affinity, dependent on F508, such that loss of F508 abolishes this link both in vitro and in the intact cell.

Keywords: Smallpox, Antigen presentation/processing, Inflammation, Mucosa, Cell surface molecules