Research > Chronic diseases, Surgery and Health Care

Research Group in Immunology and Metabolism (GRIM)

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1. Studies of the immunopathogenic mechanisms involved in the development of Autoimmune Diabetes: most studies are carried out in mouse models of human Type 1 Diabetes (TD1). It also involves the study of environmental mechanisms (e.g. constituents of the intestinal microbiota) that may trigger or, on the contrary, slow down the development of this disease. We also occasionally study samples from patients or relatives with TD1. The studies also aim to identify the internal or external elements that allow us to apply a therapy (e.g. microbiotherapy) to treat this disease.
2. Studies on the immunological mechanisms involved in the response against cancer: we analyse, in different animal models and in humans, the immune response that develops in the presence of cancer. We are currently studying an immunotherapy that we have found to be capable of boosting this natural immune response in this disease. We have focused mainly on melanoma, but our aim is to extend this immunotherapy to other types of cancer.
3. Identification of novel cyclin D3-initiated signalling pathways responsible for beta-pancreatic cell viability and function: our group has described that pancreatic islet inflammation in autoimmune diabetes causes a downregulation of cyclin D3 expression and that cyclin D3 promotes beta-cell survival and well-being in a cell cycle-independent manner. Our group investigates novel cyclin D3 signalling pathways causally related to beta cell viability and physiology as a potential source of therapeutic approaches to autoimmune diabetes.
4. Antigen-specific immunotherapy of T1DM through the use of tolerogenic dendritic cells (DCs) loaded with autoantigenic peptides (tiDCs): allogeneic pancreatic islet transplantation as a replacement therapy for the excess beta-pancreas eliminated during the autoimmune process requires the use of immunosuppressants to prevent both graft rejection and autoimmune relapse into the graft. Currently, immunosuppression is non-specific and generalised, increasing the graft recipient's risk of infections and tumour processes. Our group has developed a differentiation protocol to obtain tiDCs that promote the expansion of pancreatic autoantigen-specific regulatory/immunosuppressive T lymphocytes. In this way the immunosuppressive action remains restricted to pancreatic islets and not in the whole organism. Currently, we want to identify biomarkers of tiDCs responsible for their tolerogenic phenotype, in order to be able to intervene pharmacologically.