Immunometabolism control in chronic inflammatory diseases
I graduated from the University of Naples “Federico II” (Italy) with a degree in Medical Biotechnology in 2002 and a PhD in Molecular Oncology and Endocrinology in 2007. During my PhD I studied the pro-inflammatory and anti-apoptotic response controlled by the NF-kappaB family of transcription factors downstream of TNF receptors, upon endoplasmic reticulum stress and during tumourigenesis. In 2007 I joined the group led by Professor Guido Franzoso at the University of Chicago (USA) first and Imperial College (UK) later driven by the aspiration of gaining a better understanding of the physiopathologic relevance of inflammatory processes to a wide range of human diseases.
During that time I worked on the identification of the molecular links between inflammation and metabolism and contributed to the discovery of the control of metabolic circuitries by NF-kappaB. With the knowledge I gained of the molecular mechanisms of metabolic reprogramming in proliferating cells, I decided to focus my research interests on the emerging field of immunometabolism. I joined the WHRI in 2011 with a Lectureship in Molecular Immunology and obtained funding from the British Heart Foundation for an Intermediate Basic Science Research Fellowship with the aim of investigating the metabolic control of T cell migration and the implications of metabolic dependence of immune inflammation in physiology and chronic inflammatory disorders.
Summary of Research
Chronic inflammatory disorders (CIDs) are a leading cause of morbidity worldwide. T cell-mediated inflammation is associated with these conditions and contributes to their pathogenesis and progression. My preliminary studies indicate that interfering with metabolic pathways (i.e., lipid, glucose and oxidative metabolism) alters T cell trafficking and effector functions in vitro and in vivo. The hypothesis I am investigating is that metabolic alterations in CIDs lead to aberrant T cell migration patterns and pro-inflammatory responses, which favour the establishment of chronic inflammation.
I am exploring the mechanisms of metabolic control of T cell migration and effector functions in physiology and under metabolic stress. I am also investigating the effects of drugs that correct altered metabolism (e.g., the antidiabetic drug metformin) on T cell trafficking and inflammation in murine models of atherosclerosis, obesity and rheumatoid arthritis. These studies are providing insights into the role of energy balance on physiologic T cell trafficking and effector functions and the effect of altering metabolism on the development of T cell-mediated inflammation, as well as new therapeutic targets to prevent inflammation in CIDs.