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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 Jonsson123*

Author Affiliations

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

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

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

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


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

Published: 31 July 2008

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.