An immunohistochemical study of immunological phenomena in minor salivary glands in patients with Sjögren's syndrome

Abstract

Using different monoclonal antibodies, we performed an immunofluorescent technique on labial salivary glands in order to investigate the immunological phenomena involved in Sjögren's syndrome (SS). An aberrant expression of HLA-DR molecules was detected on cytoplasm of epithelial labial salivary cells in 9 out of 19 (47%) patients, with SS. No such expression was found in 8 patients without SS or in 3 normal controls. HLA-DQ molecules were demonstrated also in two out of ten SS patients without HLA-DR. A lymphocytic infiltration was not correlated with the expression of class II molecules. T cells bearing gamma delta receptors were not detected. The intracellular adhesion molecules (ICAM-1) and lymphocyte function associated antigen-1 (LFA-1) were not found on epithelial glandular salivary cells of patients and controls. In conclusion, these data suggested that the absence of ICAM-1 and LFA-1 in salivary cells and the absence of infiltrating T cells bearing gamma delta receptors exclude their immunopathogenetic role in SS; moreover, these data demonstrated that the aberrant expression of HLA class II molecules on epithelial salivary cells of patients with SS is not a phenomenon correlated with the lymphocytic infiltration.

Activation of epithelial and myoepithelial cells in the salivary glands of patients with Sjögren's syndrome: high expression of intercellular adhesion molecule-1 (ICAM.1) in biopsy specimens and cultured cells

“…The role of ICAM.1 in the pathogenesis of Sjogren's syndrome has been previously investigated [11–18]. Although in all previous reports, the mononuclear infiltrates appeared the principal cellular source of ICAM.1 in tissues from SS patients, ductal or acinar glandular epithelial expression has been reported in some of the studies [15–18].…”

“…Finally, epithelial type‐specific regulatory mechanisms might also participate, as implied by the differential ICAM.1 expression observed between acinar epithelial, ductal epithelial and myoepithelial cells. In this context, it may be relevant that the epithelial‐specific protein secretory component, which is reportedly over‐expressed by the salivary acinar cells of SS patients [13], may act as an intrinsic inhibitor of ICAM.1 expression [30].…”

“…Increased ICAM.1 expression has been observed, however, the cellular distribution of this expression has been controversial. Although, this has been primarily attributed to infiltrating mononuclear cells [11–18], limited ductal or acinar glandular ICAM.1 expression has been described in some studies [15–17], whereas increased glandular ICAM.1 expression has been observed in SS patients with tubulointerstitial nephritis [18]. Fortuitous preliminary immunochemical observations had indicated to us that the epithelial structures are also an important source of ICAM.1 expression in minor salivary gland biopsy samples and cultured epithelial cells from patients with SS.…”

Mucosal‐associated invariant T cells are reduced and functionally immature in the peripheral blood of primary Sjögren's syndrome patients

“…The potential role of conventional CD4 + T helper cells in the pathogenesis of SS have been reported in the recent literature . These cells are proposed to play an important role in the induction and maintenance of the disease . However, little is known regarding the involvement of mucosal‐associated invariant T (MAIT) cells in the pathogenesis of pSS.…”

Salivary dysbiosis in Sjögren’s syndrome and a commensal-mediated immunomodulatory effect of salivary gland epithelial cells

“…Modulation of immune response by SGECs is of particular interest as demonstrated by the aberrantly expressed class II MHC molecules [7][8][9][10][11][12][13][14][15] and co-stimulatory molecules [15][16][17][18][19] . SGECs also induce proliferation of anti-CD3-stimulated CD4 T cells in vitro 17,20 .…”