The Laboratory of Experimental Medicine, U.L.B. (Director : Décio L. Eizirik), is located in the research buildings of the Campus Erasme, U.L.B.. The total area of the Laboratory of Experimental Medicine is 502 m², including 9 offices, 8 large laboratories and 6 modules (cold chamber, radioactive room, FACS room, cell culture rooms and deposit). The Laboratory has presently about 25 members, including tenured scientists (associate and full professors), post-doctoral fellows, Ph.D. students, biologists, laboratory assistants, a grant administrator and a secretary.

The Laboratory of Experimental Medicine investigates the molecular pathways involved in beta-cell impairment and apoptosis in diabetes. For this purpose, members of the laboratory use state of the art methodologies, such as functional genomics, exon arrays and RNA sequencing coupled to a systems biology approach, to unveil gene networks regulated by cytokines and free fatty acids. This leads to the discovery of key "beta-cell gene modules" regulated by transcription factors such as NF-kB, STAT-1, IRF-1, IRF3 and JunB. These "gene modules" define beta-cell fate following immune- and metabolic-induced injury. Members of the laboratory have recently demonstrated that Toll-like receptor 3 and MDA5 contribute to dsRNA-induced apoptosis in pancreatic beta cells, and that PTPN2, a candidate gene for type 1 diabetes, modulates beta-cell death triggered by interferon-γ. This was the first indication that candidate genes for type 1 diabetes actually modulate apoptosis and local inflammation at the beta cell level. Members of the laboratory are presently characterizing other candidate genes for diabetes in beta cells, and defining how their interaction with environmental factors (viral infection or metabolic stress) triggers beta cell dysfunction and death, and provides signals for local inflammation (insulitis).

Another recent and exciting research area of the laboratory focuses on the role of endoplasmic reticulum (ER) stress in beta cell dysfunction and death. This led to the establishment of a global profiling of ER stress modified genes, providing new data that could pave the way to the development of strategies for the protection of pancreatic beta-cells under pathological conditions. For instance, it was shown that ER stress induces direct degradation of insulin mRNA, which has a major impact on beta cell function, and recent findings clarified the cross-talk between ER and mitochondria that regulates beta cell apoptosis.