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Editorial

Altered fractalkine cleavage results in an organ-specific 17 kDa fractalkine fragment in salivary glands of NOD mice

Nicolas Delaleu1 and Roland Jonsson1,2,3 email

Broegelmann Research Laboratory, The Gade Institute, University of Bergen, Haukelandsveien 28, Bergen 5021, Norway

Department of Rheumatology, Haukeland University Hospital, Bergen, Jonas Liesvei 65, Bergen 5021, Norway

Department of Otolaryngology, Head and Neck Surgery, Haukeland University Hospital, Bergen, Jonas Liesvei 65, Bergen 5021, Norway

author email corresponding author email

Arthritis Research & Therapy 2008, 10:114doi:10.1186/ar2458

Published: 31 July 2008


See related research by Wildenberg et al., http://arthritis-research.com/content/10/3/R69

Abstract

Sjögren's syndrome is a rheumatic disease in which the salivary and lacrimal glands are the principal targets of a pathological autoimmune reaction. Previous studies in mice indicated that delayed organogenesis and aberrant cell physiology followed by an increase in acinar cell apoptosis precede chronic focal inflammation in the salivary glands and the manifestation of impaired exocrine gland secretion. In a recent study by Wildenberg and colleagues, the authors report aberrant proteolytic activity in the salivary glands of non-obese diabetic mice and the generation of a unique organ-specific 17 kDa fragment of the chemokine and adhesion molecule fractalkine.


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