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Rheumatology Advance Access originally published online on April 19, 2005
Rheumatology 2005 44(8):965-970; doi:10.1093/rheumatology/keh647
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Published by Oxford University Press on behalf of the British Society for Rheumatology 2005.

REVIEW

Sjögren's syndrome and the danger model

A. Bredberg, G. Henriksson, Å. Larsson, R. Manthorpe and A. Sallmyr

Sjögren's Syndrome Research Centre, Department of Medical Microbiology, University Hospital UMAS, Lund University, Malmo, Sweden.

Correspondence to: A. Bredberg, Department of Medical Microbiology, University Hospital, S-20502 Malmo, Sweden. E-mail: anders.bredberg@mikrobiol.mas.lu.se

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


   Introduction
 
This review seeks to cover the data on primary Sjögren's syndrome (SS) that has accumulated especially during recent years, and that apparently fits into a common theme of cellular stress abnormalities. This includes demonstrations of hyperactivity of danger-sensing antigen-presenting cells (APC), and of a strong response to DNA damage in many different cell types. The relevance of these findings for the pathogenesis of SS will be addressed by applying them to the danger model of immune activation [1, 2].

This model has been put forward by Matzinger, stating that immune activation, including the innate system as well as the adaptive lymphocyte response, is initiated by danger in a broad sense rather than solely by the presence of infectious non-self material. By means of danger signals, tissue stress is postulated to activate the APC of the innate immune system, in turn influencing also the adaptive immune cells, i.e. . . . [Full Text of this Article]


   DNA damage: a high level in salivary glands, and an exaggerated defence reaction in SS cells
 

   High level of danger signals in SS causes exaggerated APC activity
 

   Acetylcholine deficiency may contribute to the exaggerated APC activity
 

   Can the danger model explain the preferential and chronic engagement of the salivary glands?
 

   Conclusions
 

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