A5023127754- T-cell and B-cell Immunology
- Systemic Lupus Erythematosus Research
- Immune Cell Function and Interaction
- Monoclonal and Polyclonal Antibodies Research
- Cytokine Signaling Pathways and Interactions
- Immunotherapy and Immune Responses
- Cancer Immunotherapy and Biomarkers
- Diabetes and associated disorders
- Immune Response and Inflammation
- Cell Adhesion Molecules Research
- Atherosclerosis and Cardiovascular Diseases
- Glycosylation and Glycoproteins Research
- Immunodeficiency and Autoimmune Disorders
- interferon and immune responses
- Molecular Biology Techniques and Applications
- Genetic Mapping and Diversity in Plants and Animals
- Pancreatic function and diabetes
- Cancer Genomics and Diagnostics
- Animal Genetics and Reproduction
- Chronic Lymphocytic Leukemia Research
- Animal Behavior and Reproduction
- Renal cell carcinoma treatment
- RNA modifications and cancer
- Evolution and Genetic Dynamics
- Complement system in diseases
The University of Texas Southwestern Medical Center
2015-2024
Southwestern Medical Center
2014-2024
Southwestern University
2018
Chinese Academy of Sciences
2013-2016
Shanghai Institutes for Biological Sciences
2016
Shanghai Jiao Tong University
2016
University of Florida
1995-2015
Beijing Institute of Genomics
2013-2014
The University of Texas at Austin
2012
Institute of Immunology
2005-2007
The mammalian intestine is home to ~100 trillion bacteria that perform important metabolic functions for their hosts. proximity of vast numbers host intestinal tissues raises the question how symbiotic host-bacterial relationships are maintained without eliciting potentially harmful immune responses. Here, we show RegIIIγ, a secreted antibacterial lectin, essential maintaining ~50-micrometer zone physically separates microbiota from small epithelial surface. Loss segregation in RegIIIγ(-/-)...
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of tolerance to nucleic acids and highly diverse clinical manifestations. To assess its molecular heterogeneity, we longitudinally profiled the blood transcriptome 158 pediatric patients. Using mixed models accounting for repeated measurements, demographics, treatment, activity (DA), nephritis class, confirmed a prevalent IFN signature identified plasmablast as most robust biomarker DA. We detected gradual...
The y-linked autoimmune accelerating (yaa) locus is a potent disease allele. Transcription profiling of yaa-bearing B cells revealed the overexpression cluster X-linked genes that included Tlr7. FISH analysis demonstrated translocation this segment onto yaa chromosome. resulting Tlr7 increased in vitro responses to Toll-like receptor (TLR) 7 signaling all males. B6.yaa mice are not overtly autoimmune, but addition Sle1, which contains autoimmune-predisposing Slam/Cd2 haplotype, causes...
We previously produced three congenic strains carrying lupus susceptibility genes ( Sle1-Sle3 ) from the lupus-prone NZM2410 mouse on C57BL/6 background and characterized their component phenotypes. Sle1 mediates loss of tolerance to nuclear antigens; Sle2 lowers activation threshold B cells; Sle3 a dysregulation CD4 + T cells. have now created collection bi- tricongenic with these intervals assessed autoimmune phenotypes they elicit in various combinations. Our results indicate that is key...
The major murine systemic lupus erythematosus (SLE) susceptibility locus Sle1 is syntenic to a chromosomal region linked with SLE in multiple human studies. Congenic analyses have shown that breaks tolerance chromatin, necessary step for full disease induction can be suppressed by specific modifier loci. In the present study, our fine mapping analysis of location has determined three loci within this congenic interval, termed Sle1a , Sle1b and Sle1c independently cause loss chromatin. Each...
Abstract We describe the in vivo phenotypes associated with three genomic intervals containing systemic lupus erythematosus (SLE)-susceptibility genes derived from SLE-prone NZM2410 strain on a C57BL/6 genome. These were identified previously via genome-wide analysis of SLE susceptibility (NZM2410 x C57BL/6)F1 backcross, and transferred independently background to produce congenic strains: B6.NZMc1 carrying Sle1, B6.NZMc4 Sle2, B6.NZMc7 Sle3. develops high titers IgG anti-nuclear...
FcγRIIB is a potent lupus susceptibility gene as demonstrated by the observation that mice deficient in this molecule develop spontaneous antinuclear antibodies (ANA) and fatal glomerulonephritis when on C57BL/6 background. To determine mechanisms underlying epistasis displayed we have constructed hybrids between FcγRIIB−/− systemic erythematosus (SLE) modifiers yaa lpr locus Sle1. Sle1 B6.RIIB−/− are both physically functionally coupled; compound heterozygotes of significant disease, while...
The susceptibility locus for the autoimmune disease lupus on murine chromosome 1, Sle1z/Sle1bz, and orthologous human are associated with production of autoantibody to chromatin. We report that presence Sle1z/Sle1bz impairs B cell anergy, receptor revision, deletion. Members SLAM costimulatory molecule family constitute prime candidates Sle1bz, among which Ly108.1 isoform Ly108 gene was most highly expressed in immature cells from lupus-prone B6.Sle1z mice. normal Ly108.2 allele, but not...
Susceptibility to systemic lupus erythematosus in the NZM2410 murine model maps Sle1, Sle2, Sle3, and H2 loci. To unravel how these loci contribute pathogenesis of lupus, individual NZM2410-derived genomic intervals bearing have been successfully backcrossed onto resistant C57BL/6 (B6) background. The focus this study was understand Sle2 on chromosome 4 impacts immune system. Compared with mice, B6 mice congenic for exhibit a variety immunophenotypes affecting their B cells. They an early,...