Objective. Many studies have shown that the microanatomic organization of infiltrating leukocytes in the salivary gland lesions of patients with Sjögren's syndrome (SS) resembles the structure of lymphoid organs. A newly defined set of chemokines referred to as "lymphoid," which orchestrate leukocyte microenvironmental homing and contribute to the formation of lymphoid structures, provides directional clues. The aim of this study was to investigate the possible existence of "lymphoid" chemokines in the chronic inflammatory lesions of SS patients and thus validate their potential involvement in the disease process.Methods. Twelve patients with primary SS, 3 patients with secondary SS, 4 patients with other autoimmune disorders, and 4 control individuals were the subjects of this study. Reverse transcriptasepolymerase chain reaction analysis was performed in order to examine the messenger RNA (mRNA) expression of "lymphoid" chemokines. Furthermore, in situ hybridization studies revealed chemokine mRNA localization. Immunohistochemistry was also applied in order to identify the cell types that expressed the chemokine mRNA.Results. STCP-1/monocyte-derived chemokine and TARC mRNA were expressed in the majority of patients with primary and secondary SS, in 2 of 4 patients with other autoimmune disorders, and in 2 of 4 controls. BCA-1, ELC, and PARC mRNA were only detected in patients with primary and secondary SS. SLC mRNA was also detected in 1 non-SS patient. The main cellular sources of chemokine mRNA were ductal epithelial cells and infiltrating mononuclear leukocytes.Conclusion. The expression pattern of "lymphoid" chemokine mRNA points further to the role of epithelial cells in the pathogenesis of SS and offers new insight into the potential mechanisms that could be involved in leukocyte attraction and in the in situ formation of secondary lymphoid tissue structures.
Objective. To investigate the expression of B7 costimulatory molecules in the lymphoepithelial lesions of salivary gland (SG) biopsy tissues and in SG epithe-lial cell lines derived from patients with Sjögren's syndrome (SS). Methods. B7.1 and B7.2 protein expression was studied by immunohistochemistry in minor SGs obtained from 11 patients with SS and 10 disease control patients with nonspecific sialadenitis and in cultured SG epithelial cell lines obtained from minor SGs from 15 SS patients and 15 control patients. B7.1 and B7.2 messenger RNA (mRNA) expression by SG epithelial cell lines was examined by reverse transcription-polymerase chain reaction (RT-PCR). Results. In biopsy tissues from SS patients, but not control patients, ductal and acinar epithelial cells showed increased expression of both B7.1 and B7.2. Intense spontaneous B7.1 protein expression (as well as HLA-ABC, but not B7.2 or HLA-DR) was also found in 73% of SG epithelial cell lines from SS patients versus 13% of those from control patients (P < 0.01). Interferon-treatment induced, or up-regulated, B7.1, B7.2, and HLA-DR expression in all SG epithelial cell lines tested. B7.1 and B7.2 expression by SG epithelial cell lines was also verified at the mRNA level by RT-PCR. Conclusion. Human SG epithelia are intrinsically capable of expressing B7 proteins upon activation. In SS patients, the expression of B7 molecules by SG epithe-lial tissues and by SG epithelial cell lines indicates the activated status of SG epithelial cells in this disorder and, possibly, their capacity for presenting antigens to T cells.
Oral lesions were significantly reduced in patients on PI-HAART. A direct anticandidal effect of PI was suggestive and seemed to have accounted, beyond the HAART-related immune reconstitution, for the reduction of candidiasis and all other oral lesions.
No significant,difference could be detected concerning the dental and periodontal status of SS patients, compared with that of patients with other immune diseases as well as with that of controls who had subjective xerostomia.
The aims of the study were (a) to investigate the prevalence of Sjögren's-like syndrome (SLS) in an unselected population of HIV-1-positive patients and (b) to describe the pathology and immunopathology of the labial minor salivary gland biopsy. Seventy-seven HIV-1-positive patients were asked to answer the validated questionnaire of the European preliminary criteria for the classification of Sjögren's syndrome on oral and ocular sicca symptoms. Twenty-six patients gave one positive answer to both ocular and oral symptoms, and of these 14 (hepatitis C virus negative) consented to participate in the study (patients group). Ten age- and sex-matched HIV-1-positive patients with a negative questionnaire constituted the control group. Patients and controls had: (a) Schirmer's test and slit-lamp examination after Rose Bengal staining; (b) parotid gland scanning with technetium; (c) detection of autoantibodies in sera to Ro/SSA and La/SSB; (d) labial salivary gland biopsy (patients group only). The control group gave negative parotid gland scanning and only one gave a positive Rose Bengal staining test. In the patients group, parotid gland enlargement was manifested by three patients and only one gave positive Rose Bengal staining test. Six out of the 14 patients had biopsies identical with Sjögren's syndrome and five of these gave positive parotid gland scanning. In the biopsies of four other patients, mucoid degeneration of the stroma was found. Immunopathology revealed that the predominant cells were T cells with the CD8 phenotype. None of the patient and control sera had autoantibodies to Ro/SSA and La/SSB, whereas all patients had hypergammaglobulinaemia. The overall prevalence of possible SLS in a mixed population of HIV(+) patients (88.3% men and 11.7% women) was 7.79% which is >2.5 times higher than that observed in normal Greek adult females.
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