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Rheumatology Advance Access originally published online on April 4, 2006
Rheumatology 2006 45(7):792-798; doi:10.1093/rheumatology/kel067
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

REVIEW

Sjögrens syndrome—the non-apoptotic model of glandular hypofunction

L. J. Dawson, P. C. Fox1 and P. M. Smith

Sjögren's Syndrome Research Group, The University of Liverpool School of Dentistry, Liverpool, UK and 1 Visiting Scientist, Department of Oral Medicine, Carolinas Medical Center, Charlotte, North Carolina, USA.

Correspondence to: L. J. Dawson, Lecturer in Oral Surgery, University of Liverpool Dental School, Room 1.10, Edwards Building, Daulby Street, Liverpool L69 3GN, UK. E-mail: ldawson@liv.ac.uk

KEY WORDS: Sjögrens syndrome, Glandular hypofunction, Mechanisms, Stimulus-secretion coupling, Antimuscarinic antibodies, Aquaporins, Cytokine

The first 150 words of the full text of this article appear below.


   Introduction
 
The ‘classical’ model to explain glandular hypofunction in Sjögrens syndrome (SS) is tissue loss secondary to immune attack mediated by a combination of apoptosis and cytotoxic cell death (reviewed recently by Ramos-Casals and Font [1]). In this model, the process of glandular destruction is made self-sustaining by the continued production of novel ‘self’ antigens, secondary to apoptotic bleb formation or cell-death [2]. Failure of the organ is thought to follow directly from tissue loss. For over six decades, research into SS has been directed towards understanding the mechanisms of destruction of salivary and lacrimal acinar tissue. Over this time, the only role envisaged for salivary glands themselves in the pathological process, has been that of a ‘reactor’ for infiltrating lymphocytes.

Three recent observations cast a serious doubt on the principles upon which the classical model for salivary gland hypofunction in SS is based. Firstly, . . . [Full Text of this Article]

A useful model for stimulus-secretion coupling in salivary acinar cells
Mechanisms of immune-induced acinar hypofunction under investigation
Receptor activation
Mobilization of Ca2+
Fluid movement
The non-apoptotic model of glandular hypofunction

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