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: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:To study the gene expression profile of salivary glands with varying degrees of inflammation in Sjogren's and non Sjogren's patients
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: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:To study the gene expression profile of salivary glands with varying degrees of inflammation in Sjogren's and non Sjogren's patients Total mRNA was extracted from whole minor salivary glands of patients with SS and control
Project description:Genome-wide association studies of Systemic Lupus Erythematosus (SLE) nominate 3,073 genetic variants at 91 risk loci. To systematically screen these variants for allelic transcriptional enhancer activity, we constructed a massively parallel reporter assays (MPRA) library comprising 12,396 DNA oligonucleotides containing the genomic context around every allele of each SLE variant. Transfection into Epstein-Barr virus-transformed B cell line GM12878 revealed 482 variants with enhancer activity, with 51 variants showing genotype-dependent (allelic) enhancer activity at 27 risk loci. Combined with allelic enhancer activity analyses in Jurkat cell line, we identified shared and unique allelic transcriptional regulatory mechanisms at SLE risk loci. In-depth analysis of allelic transcription factor (TF) binding at and around 51 allelic variants identified one class of TFs whose DNA-binding motif tends to be directly altered by the risk variant and a second, larger class of TFs that also bind allelically but do not have their motifs directly altered by the variant. Collectively, our approach provides a blueprint for the discovery of allelic gene regulation at risk loci for any disease and offers insight into the transcriptional regulatory mechanisms underlying SLE.