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Biography

daniele-corridoni.jpgI obtained a Medical Biotechnology degree (2005) followed by a Masters degree in Pharmaceutical and Medical Biotechnology (2008) at the University of L’Aquila (Italy). In 2008, I started my Ph.D. in Internal Medicine and Immunology at the University of L’Aquila studying innate immune processes related to the pathogenesis of chronic inflammatory diseases. During the second year of my Ph.D., I was selected to continue my project at Case Western Reserve University in the Digestive Health Research Center (Cleveland, USA), as part of a Ph.D. program in Italy that allows graduate students to perform a portion of their research project in a foreign laboratory to acquire new skills and learn new techniques. During that period, I completed my work on the mechanisms of action of probiotics in mouse models of ileitis. I obtained my Ph.D. degree in April 2012. I then started a post-doctoral fellowship at Case Western Reserve University working on a project investigating the role of NOD2 signaling in the pathogenesis of Crohn’s Disease (CD)-like ileitis. Briefly, we discovered that SAMP1/YitFc (SAMP) mice, which develop spontaneous and progressive CD-like ileitis, display dysregulated intestinal innate immunity related to the NOD2 signaling that may have pathogenic relevance, at least in a subgroup of patients with CD. In addition, we demonstrated that NOD2 plays a dual role in the pathogenesis of CD-like ileitis, by protecting the intestinal mucosa under normal physiological conditions and inducing high production of pro-inflammatory cytokines during the chronic phase of gut inflammation.

After 6 years in the States, I’ve recently moved to the UK to work under the supervision of Prof. Alison Simmons at the University of Oxford. By using large-scale screening techniques, such as phospho-proteomic analysis, we are exploring how the activation of innate immune sensors, including NLRs and TLRs, form signaling platforms in primary human cells required for bacterial degradation, antigen cross-presentation and priming of specific T-cell subsets. This work will define novel molecular and cellular features of innate immune defense in response to commensal flora or pathogenic bacteria and describe how these mechanisms might be affected in inflammatory bowel disease (IBD) or inflammation-associated cancer, with the ultimate goal to highlight new therapeutic targets which could translate to putative clinical pharmacotherapy.