An 11‐year prospective study was carried out in 226 patients with organ‐specific autoimmune disease (OSAD) coming from northern Italy and southern England. Patients were investigated for diabetes‐related autoantibodies (ICAs, GADAbs, and IA2Abs) in order to evaluate the best immunological combination in predicting type 1 DM. One hundred twenty‐eight patients were ICA positive (77 Italian and 51 English), and 98 were ICA negative. ICAs were detected by immunofluorescence technique on human pancreas, whereas GADAbs and IA2Abs were found by immunoprecipitation assay. During follow‐up, 33 of 128 (25.8%) ICA+ (26% of Italian and 25.5% of English) and 2 of 98 (2%) ICA− patients developed type 1 DM (17 with acute‐onset, and 18 with non‐acute‐onset disease). Among ICA+ patients, three subgroups were considered: ICA+ alone; ICA and GADAb+; ICA, GADAb, and IA2Ab+. Patients who were only ICA+ had a predictive value for type 1 DM of 4.7%, with an annual incidence of 0.7%, and a cumulative risk of 6%. ICA and GADAb+ patients had a predictive value of 17.5%, with an annual incidence of 2%, and a cumulative risk of 20%. ICA, GADAb, and IA2Ab+ patients had a predictive value of 72, with an annual incidence of 13%, and a cumulative risk of 87%. Patients having three immunological markers revealed a prevalence increased in HLA‐DR3 and/or ‐DR4, but reduced in HLA‐DR2 haplotypes. The risk for type 1 DM increased proportionally with the number of diabetes‐related antibodies, which were also related to the presence of genetic markers of disease susceptibility.
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.
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