Pattern of adhesion molecule expression in labial salivary glands from patients with primary Sjögren's syndrome

The aim of this work was to examine the pattern of distribution of adhesion molecules in minor salivary glands from patients with primary Sjögren's syndrome (SS). Labial salivary gland (LSG) biopsies from 31 patients with primary SS and 21 normal subjects were examined. Cryostat sections were examined with monoclonal antibodies to different adhesion molecules using an indirect immunoperoxidase technique. There was an increased expression of ICAM-1, class IMHC, HLA-DR & DQ (p<0.05) on endothelial cells, lymphocytes, fibroblasts and salivary epithelial cells (HLA-DR far exceeds ICAM-1 (limited) epithelial expression). ELAM-1 and to a lesser extent VCAM-1 were demonstrated over some of the endothelial cells in patients, but not in controls (p<0.01). Many of the endothelial cells expressing ICAM-1, DR, DQ, ELAM-1 were high endothelial venules. CD44 was strongly expressed over epithelial cells, endothelial and infiltrating mononuclear cells, while LFA-3 was present mainly on epithelial cells, and faintly on infiltrating inflammatory cells. There was no difference between patients and controls with regard to CD44 or LFA-3 expression. The ligands for the above mentioned adhesion molecules, namely LFA-1α, LFA-1ß, LECAM-1, VLA-4ß(CD49d), CD44 and CD2 were demonstrated (variably) on the surface of infiltrating lymphocytes. CD11b and CD11c were detected over monocytes/macrophages. A proportion of lymphocytes expressed VCAM-1 and CD11c and may function as antigen presenting cells. In some biopsies these molecules were localized at the center of lymphoid follicles with the appearance of dendritic cells. Although the majority of lymphocytes were activated and strongly expressing DR and ICAM-1, they were IL-2Rα (CD25) negative. We conclude that adhesion molecules are prominent in LSG of patients with primary SS. They may play a major role by mediating the lymphocytic infiltration to the glands, retaining the lymphocytes in the glands and regulating the different immune responses in the local microenvironment of this chronic inflammatory disease.