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Our research investigates the differentiation and function of natural killer T (NKT) lymphocytes, using models for infection and autoimmune diseases. The aim is to determine regulatory features and effector mechanisms of these innate-like lymphocytes in the context of inflammation and infection. Our long term goal is to acquire knowledge that can be used to design immunotherapies to modulate harmful or insufficient immunity.
Natural killer T (NKT) lymphocytes make up a subset of T lymphocytes, which is activated by glycolipid antigens presented on the non-classical MHC class I like molecule CD1d. They are associated with early immune responses and immune regulation, and are regarded as part of a crucial first line of defense which bridges the innate and adaptive immune response. NKT cells regulate the immune response in diverse situations, such as autoimmune diseases in humans and mice, tumor rejection and different types of infections.
Several reports have shown that CD1d-restricted natural killer (NK) T cells can protect against experimentally induced or spontaneous autoimmune disease in the mouse. The disease which has been most well investigated in this respect is autoimmune or Type 1 diabetes (T1D). We investigate the regulatory role of NKT cells in the non obese diabetic (NOD) mouse strain, which develops a spontaneous Type 1 Diabetes very similar to the human disease. The glycolipid ligands of NKT cells are still poorly characterized, and we attempt to define additional ligands using our unique NKT cell-lines. We are also investigating further the previously identified ligand sulfatide, sulfatide specific CD1d-restricted NKT cells, their role in the pathogenesis of inflammatory demyelinating diseases.