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Rheumatology 2000; 39: 119-121
© 2000 British Society for Rheumatology

Editorial

Apoptosis—new clues to the pathogenesis of Sjögren's syndrome?

Y. I. Patel and N. J. McHugh1

Groote Schuur Hospital and University of Cape Town, J47 Old Main Building, Groote Schuur Hospital, Cape Town, South Africa and
1 Royal National Hospital for Rheumatic Diseases, Upper Borough Walls, Bath BA1 1RL, UK

Sjögren's syndrome (SS), characterized clinically by xerostomia and xerophthalmia, is associated with a destruction of glandular tissue and a resultant impaired secretory capacity of mainly salivary and lacrimal glands. In addition, salivary gland samples from patients with SS show characteristic mononuclear cell infiltrates centred around the feeding vessels of glandular lobules, often in myoepithelial islands and germinal centre-like structures. The mononuclear infiltrates consist predominantly of T cells (CD4 > CD8), with some B cells and plasma cells. Glandular attrition is largely restricted to the acinar and ductal epithelial cells and there is progressively less destruction in the periphery of lobules than around the central blood vessels [1]. Interestingly, this pattern of centri-lobular destruction is also associated with the highest number of lymphocytic infiltrates, suggesting either an attraction of lymphocytes to the area by adhesion molecules and/or that the lymphocytes mediate . . . [Full Text of this Article]

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