Expression of Selectins (CD62 E,L,P) and Cellular Adhesion Molecules in Primary Sjögren's Syndrome: Questions to Immunoregulation

作者: Karim Elias Aziz , Peter J. McCluskey , Denis Wakefield

DOI: 10.1006/CLIN.1996.0094

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摘要: Adhesion molecules are important signal transmitters of the immune system and may mediate homing leukocytes to sites inflammation. The aim this work was examine presence selecting cellular adhesion on epithelial endothelial cells in labial salivary glands (LSG) Sjogren's syndrome (SS). LSG biopsies were obtained from patients with primary SS (n = 31) normal subjects 21). Cryostat sections examined indirect immunoperoxidase. Epithelial both controls expressed LFA-3 (CD58) Hermes I (CD44). A significantly increased number acinar ductal class MHC (74%, as mean percentage cells) (P < 0.05), HLA-DR (58%) 0.0001), HLA-DQ (11%) 0.001). To a lesser extent limited ICAM-1 (CD54) expression (6%) noted only few but none controls. did not express any selectins CD62 E, L, P sometimes they sialyl Le(x) (a ligand for selectins). Although structures expressing (CD54), HLA-DR, HLA-DQ, (per surface area) be due total increase 0.05) (Von Willebrand factor +ve) part chronic inflammatory process. smaller proportion E-selectin (CD62 E) (32%) VCAM-1 (CD106) (approximately 7%) detectable some patients. P-selectin P) demonstrated about one-third Infiltrating mononuclear CD11a (68%), CD18 (73%), CD11b (13%), CD11c (21%), CD58 CD4 (44%), CD8 (17%), CD62L (L-selectin) (18%), CD49d (38%), CD49e (15%), CD2 (56%), CD44 (77%). relatively reduced L +ve lymphocytes shedding that molecule after activation. Sialyl infiltrating lymphocytes. activated, evidenced by their (72%) (55%), IL-2Ralpha (CD25, confirmed two antibodies 2A3 ACT1) or IL-2Rbeta (CD122), except rarely (< 1%). In biopsies, CD106 localized at central areas periductal lymphoid follicles appearance dendritic cells. We conclude probably play major role pathogenesis SS. pattern these demonstrates regulated altered activation associated disease. subject specific regulatory factors, addition proinflammatory cytokines.

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