Project description:We performed autoantigen arrays on sera derived from Sjogren's syndrome mice that lacked Myd88 systemically (NOD.B10LSL-/- strain) or lacked Myd88 in specific tissues (NOD.B10Myd88delta and NOD.B10LSL-/-Vav+ strains). We also examined sera from Myd88-sufficient controls (NOD.B10Myd88fl/fl, NOD.B10, and NOD.B10LSL+/- strains).
Project description:Sera were acquired from the Sjogren's International Collaborative Clinical Alliance (SICCA) biorepository and were assayed for IgG autoantibodies. The autoantigen array was performed to identify the specific autoantibodies that were enriched in pSS patients.
Project description:Spleens (n = 2-3) were harvested from mice with primary Sjogren's syndrome (NOD.B10) and cells were sort-purified. Follicular B cells (FO) (6 million), Marginal zone B cells (4.5 million) and age-associated B cells (500,000) were sorted. Cells were cultured in 200 uL of complete RPMI media containing 62.5 ng/mL of imiquimod, a TLR7 agonist. Cells were cultured for 6 days, and the supernatants were harvested and stored at -20 C. Samples were shipped to UT Southwestern for autoantigen array analysis.
Project description:A study was designed to further define the viral landscape within Sjogren's Syndrome (pSS) affected salivary gland tissue to identify potential viral-mediated triggers in the pathogenesis of this autoimmune disease.
Project description:A study was designed to further define the viral landscape within Sjogren's Syndrome (pSS) affected salivary gland tissue to identify potential viral-mediated triggers in the pathogenesis of this autoimmune disease. Viral Probes for Vertebrate Infecting Viral Families
Project description:To study the gene expression profile of salivary glands with varying degrees of inflammation in Sjogren's and non Sjogren's patients
Project description:Abstract Objective: To identify neuronal surface antibodies in opsoclonus myoclonus ataxia syndrome (OMAS) with contemporary antigen discovery methodology. Methods: OMAS patient serum IgG immunohistochemistry using age-equivalent rat cerebellar tissue was followed by immunoprecipitation, gel electrophoresis and mass spectrometry generated a list of potential neuronal surface cerebellar autoantigens. Live cell-based assays (CBA) were used to confirm membrane-surface antigens and adsorb antigen-specific IgGs. The serological results were compared to the clinical data. Results: Four of the six OMAS sera tested bound rat cerebellar sections. Two of these sera with similar immunoreactivities against rat cerebellar sections were used in immunoprecipitation experiments using cerebellum from postnatal rat pups (P18). Mass spectrometry identified 12 cell-surface proteins, of which glutamate receptor delta 2 (GluD2), a predominately cerebellar-expressed protein, was found at a threefold higher concentration than the other 11 proteins. Antibodies to GluD2 were identified in 14/16 (87%) OMAS samples, compared with 5/139 (5%) pediatric and 1/38 (2.6%) adult serum controls (p<0.0001), and in 2/4 sera from patients with neuroblastoma without neurological features. Adsorption of positive OMAS sera against GluD2-transfected cells substantially reduced but did not eliminate, reactivity towards cerebellar sections. Conclusion: Autoantibodies to GluD2 are frequent in patients with OMAS, bind to surface determinants and are potentially pathogenic.