Disease relevance of Sjogren's Syndrome

• Aseptic meningitis, trimethoprim, and Sjögren's syndrome [1].
• Anti-Ro60 autoantibodies are found in a variety of autoimmune disorders including systemic lupus erythematosus (SLE), Sjögren's syndrome, primary biliary cirrhosis, and active hepatitis [2].
• Many lupus and Sjögren's syndrome patients, as well as most neonatal lupus infants with congenital heart block or dermatitis, have antibodies to the ribonucleoprotein Ro/SSA, which is one of a group of RNA-protein autoantigens commonly found in human lupus sera [3].
• Immunologic and structural studies of the lupus/Sjögren's syndrome autoantigen, La/SSB, with a monoclonal antibody [4].
• Fresh PBLs were isolated from patients with IDDM, Hashimoto's thyroiditis, Graves' disease, systemic lupus erythematosis, rheumatoid arthritis, and Sjogren's syndrome [5].

Psychiatry related information on Sjogren's Syndrome

• Certain systemic diseases such as Sjögrens syndrome, rheumatoid arthritis and anorexia nervosa which have specific oral manifestations are especially common in women [6].

High impact information on Sjogren's Syndrome

• We found immune interferon in the serums of patients with systemic lupus erythematosus, rheumatoid arthritis, scleroderma and Sjögren's syndrome [7].
• To determine whether Sjögren's syndrome is primarily associated with an HLA-D antigent or with HLA-A and HLA-B antigens as well as HLA-Dw3, which is known to be in linkage disequilibrium with HLA-B8 [8].
• We found the primary association of association of Sjögren's syndrome to be with HLA-Dw3, which we observed in 84 percent of patients with Sjögren's syndrome in the absence of rheumatoid arthritis as compared to 24 percent in controls (P less than 0.00001) [8].
• We measured salivary beta2 microglobulin concentrations in 49 patients evaluated for Sjögren's syndrome with a labial salivary-gland biopsy [9].
• Beta2 microglobulin and lymphocytic infiltration in Sjögren's syndrome [9].

Chemical compound and disease context of Sjogren's Syndrome

• Sicca syndrome in a patient with toxic reaction to busulfan [10].
• Epirubicin-induced primary Sjögren's syndrome [11].
• The prevalence of different antinuclear antibodies was examined in systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, progressive systemic sclerosis, dermatomyositis, discoid lupus erythematosus, and mixed connective tissue disease [12].
• Development of autoimmune exocrinopathy resembling Sjögren's syndrome in estrogen-deficient mice of healthy background [13].
• Dehydroepiandrosterone versus placebo for Sjögren's syndrome: comment on the article by Pillemer et al [14].

Biological context of Sjogren's Syndrome

• One gene, two transcripts: isolation of an alternative transcript encoding for the autoantigen La/SS-B from a cDNA library of a patient with primary Sjögrens' syndrome [15].
• SS-A/Ro is a nucleocytoplasmic ribonucleoprotein (RNP) particle that is a common target of autoimmune response in Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE) [16].
• To investigate the temporal relationship of antibody responses to different La epitopes, sequential sera from nine patients with systemic lupus erythematosus and Sjogren's syndrome were tested by enzyme-linked immunosorbent assay for antibody binding to a series of recombinant fusion proteins containing different regions of the La molecule [17].
• This paper outlines the clinical, serologic, and immunogenetic differences and similarities of Sjögren's syndrome alone (primary) and Sjögren's syndrome associated with rheumatoid arthritis and systemic lupus erythematosus (secondary) [18].
• The rheumatic disease controls (rheumatoid arthritis; primary Sjögren syndrome; n = 8) exhibited a mean 72%, 124%, and 85%, respectively, of phosphorylation observed in healthy T cells [19].

Anatomical context of Sjogren's Syndrome

• Elevated salivary and synovial fluid beta2-microglobulin in Sjogren's syndrome and rheumatoid arthritis [20].
• In this issue of Immunity, Li and colleagues suggest an important role for Id3 function in T cell development and Sjogren's Syndrome [21].
• Here, we show that Id3-deficient mice develop many disease symptoms found in primary Sjogren's syndrome patients including dry eyes and mouth, lymphocyte infiltration in lachrymal and salivary glands, and development of anti-Ro and anti-La antibodies [22].
• Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome [23].
• Defective cellular trafficking of lacrimal gland aquaporin-5 in Sjögren's syndrome [24].

Gene context of Sjogren's Syndrome

• Increased salivary gland tissue expression of Fas, Fas ligand, cytotoxic T lymphocyte-associated antigen 4, and programmed cell death 1 in primary Sjögren's syndrome [25].
• OBJECTIVE: Previous findings in labial salivary glands (LSGs) from patients with Sjögren's syndrome (SS) suggest that increased activity and expression of matrix metalloproteinase 9 (MMP-9) and MMP-3 trigger the destruction of acinar structures in these glands [26].
• Increased acinar damage of salivary glands of patients with Sjögren's syndrome is paralleled by simultaneous imbalance of matrix metalloproteinase 3/tissue inhibitor of metalloproteinases 1 and matrix metalloproteinase 9/tissue inhibitor of metalloproteinases 1 ratios [26].
• To better define the genetic factors that predispose to primary Sjögren's syndrome (SS), we have used polymerase chain reaction in combination with oligonucleotide probe hybridization and DNA sequencing to analyze HLA-DRB1, -DQA1, -DQB1, and -DPB1 alleles in Caucasoid (California), Japanese (Tokyo), and Chinese (Shanghai and Beijing) SS patients [27].
• Dysregulation of chemokine receptor expression and function by B cells of patients with primary Sjögren's syndrome [28].

Analytical, diagnostic and therapeutic context of Sjogren's Syndrome

• By use of a radioimmunoassay, elevated concentrations of beta2--microglobulin were found in saliva and synovial fluid from patients with Sjogren's syndrome and rheumatoid arthritis, autoimmune inflammatory diseases that attack and destroy the salivary glands and articular tissues, respectively [20].
• The serum from a patient with Sjögren's syndrome (RM serum) showing a very high reactivity to the Golgi complex has been shown to immunoprecipitate and to immunodetect by Western blotting experiments a protein mol wt 210,000 (p210) that was shown to be peripheral and cytoplasmically disposed [29].
• Results of serological tests and human leukocyte antigen typing were not similar to those described in patients with primary Sjögren's syndrome but were similar to those described in patients with rheumatoid arthritis and Sjögren's syndrome [30].
• In this study, we report an established and characterized animal model for primary Sjögren's syndrome in NFS/sld mutant mice bearing an autosomal recessive gene with sublingual gland differentiation arrest [31].
• METHODS: Molecular techniques were used for HLA typing of 219 white patients with systemic lupus erythematosus and 125 white patients with primary Sjögren's syndrome [32].

References