News and Announcements
Computational modeling uncovers new molecular mechanisms controlling T helper cell function
BLACKSBURG, Va., April 04, 2013 – Researchers at the Center for Modeling Immunity to Enteric Pathogens (MIEP) at Virginia Bioinformatics Institute (VBI) believe they have identified the mechanism that turns pro-inflammatory Th17 cells into anti-inflammatory T regulatory cells in the gut. This marks the first time that a comprehensive computational and mathematical model of the mechanisms governing Th cell differentiation has been created and key model-derived predictions have been validated experimentally. The results are published in PLOS Computational Biology. The study focuses on PPAR γ, a protein that aids in metabolic regulation. In previous work, researchers at VBI’s Nutritional Immunology and Molecular Medicine Laboratory (NIMML) demonstrated that PPAR γ plays a crucial role in suppressing inflammation and immune responses. The new model developed by the MIEP team predicted a novel role of PPAR γ in controlling how gut-associated Th cells change from pro-inflammatory to anti-inflammatory types. [More ...]
Researchers identify a potential new therapeutic target for E. coli infections
BLACKSBURG, Va., March 06, 2013 – A new study by researchers at the Center for Modeling Immunity to Enteric Pathogens (MIEP) at Virginia Bioinformatics Institute provides novel insight into how enteroaggregative Escherichia coli, also known as EAEC, interacts with its host. This new knowledge could be used by scientists to devise new therapeutic strategies against E.coli. The study was published in PLOS One. EAEC infection is the most common cause of persistent diarrhea worldwide and is most frequently seen in malnourished children living in developing countries. Because these children are unable to mount an effective immune response to the bacteria, the infection often persists once it gains a foothold. A 2011 outbreak in northern Germany received international attention when it sickened more than 3,000 people, causing 53 deaths. “In many parts of the world, the relationship between infection and malnutrition is a vicious cycle. For example, malnourished EAEC-infected individuals experience a chronic burden linked to growth retardation. Our study in mice suggests that promoting inflammation may help clear the bacterial infection soon after infection,” said Josep Bassaganya-Riera, a professor of immunology, director of the Nutritional Immunology and Molecular Medicine Laboratory and the principal investigator of MIEP. [More ...]
Press Releases
- Computational modeling uncovers new molecular mechanisms controlling T helper cell function
- Researchers identify a potential new therapeutic target for E. coli infections
- ‘Villain’ gut bacteria may help control diabetes
- Research on Clostridium difficile infection yields promising new drug target
- MIEP helps bridge the immunology research community and science teachers
- MIEP team attends Modeling Immunity for Biodefense symposium
- Center for Modeling Immunity to Enteric Pathogens Releases a Revolutionary Modeling and Simulation Software: ENteric Immunity SImulator
- Center for Modeling Immunity to Enteric Pathogens Contributes Code to The Open Source Community
Selected Publications
- Animal models of enteroaggregative Escherichia coli infection
- Systems modeling of molecular mechanisms controlling cytokine-driven CD4+ T cell differentiation and phenotype plasticity
- The Role of Peroxisome Proliferator-Activated Receptor γ in Immune Responses to Enteroaggregative Escherichia coli Infection
- Helicobacter pylori colonization ameliorates glucose homeostasis in mice through a PPAR γ-dependent mechanism
- Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile
- ENISI Visual, an Agent-based Simulator for Modeling Gut Immunity
Research Highlights
Investigators in MIT and Harvard Medical School combined transcriptional profiling at high temporal resolution with high throughput strategies to identify and validate 39 regulatory factors involved in Th17 differentiation
Th17 is a proinflammatory T-cell subset that has been implicated in the pathogenesis of multiple autoimmune and infectious diseases. However, the molecular circuits that control Th17 keep largely unknown. Nir Yosef et al. in the Kuchroo Laboratory identified and validated 39 regulatory factors involved in the induction, expansion, maintenance and suppression of the Th17 phenotype within the CD4+ T cell subset. Yosef et al. embedded those factors in a comprehensive temporal network and they revealed their organizational principles. [more ...]
