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Sjögren's syndrome.


Delaleu, N; Jonsson, R; Koller, M M (2005). Sjögren's syndrome. European Journal of Oral Sciences, 113(2):101-113.

Abstract

Sjögren's syndrome (SS) is a chronic autoimmune disease affecting the exocrine glands, primarily the salivary and lacrimal glands. It has been suggested that exogenous agents may trigger SS in genetically predisposed individuals. However, at present, the etiology of SS is far from being understood, and no direct evidence for any of these triggers has been presented. The salivary and lacrimal glands from patients with SS harbor unique and highly selected T- and B-cell populations. Disturbance in glandular cell apoptosis may be one possible explanation for the sicca symptoms in SS. However, discrepancies between glandular destruction and salivary flow give rise to processes causing glandular dysfunction preceding or triggering glandular cell destruction. Recent reports suggested autoantibodies inhibiting neuronal innervation of acinar cells and defective water transport to be implicated in salivary secretion deficiency observed in SS. Several types of autoantibodies have been suggested to contribute to the pathogenesis of SS. However, how the tolerance to these structures is broken down is unknown at present. Studies on B-cell activating factor indicated that diminished apoptosis and disturbed B-cell maturation could be responsible for the occurrence of autoreactive B-cells and B-cell hyperreactivity. B-cell activation may also provide a basis for lymphoma development observed in up to 5% of the patients with SS.

Abstract

Sjögren's syndrome (SS) is a chronic autoimmune disease affecting the exocrine glands, primarily the salivary and lacrimal glands. It has been suggested that exogenous agents may trigger SS in genetically predisposed individuals. However, at present, the etiology of SS is far from being understood, and no direct evidence for any of these triggers has been presented. The salivary and lacrimal glands from patients with SS harbor unique and highly selected T- and B-cell populations. Disturbance in glandular cell apoptosis may be one possible explanation for the sicca symptoms in SS. However, discrepancies between glandular destruction and salivary flow give rise to processes causing glandular dysfunction preceding or triggering glandular cell destruction. Recent reports suggested autoantibodies inhibiting neuronal innervation of acinar cells and defective water transport to be implicated in salivary secretion deficiency observed in SS. Several types of autoantibodies have been suggested to contribute to the pathogenesis of SS. However, how the tolerance to these structures is broken down is unknown at present. Studies on B-cell activating factor indicated that diminished apoptosis and disturbed B-cell maturation could be responsible for the occurrence of autoreactive B-cells and B-cell hyperreactivity. B-cell activation may also provide a basis for lymphoma development observed in up to 5% of the patients with SS.

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Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > Center for Dental Medicine > Clinic for Masticatory Disorders
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:1 April 2005
Deposited On:11 Feb 2008 12:23
Last Modified:19 Feb 2018 19:51
Publisher:Wiley-Blackwell
ISSN:0909-8836
OA Status:Closed
Publisher DOI:https://doi.org/10.1111/j.1600-0722.2004.00183.x
PubMed ID:15819815

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