We study lymphoma and neuroblastoma in children. The cause of neuroblastoma is thought to lie in abnormal development of so-called embryonic neural crest cells. What happens is that tumor cells are able to camouflage and escape immuno surveillance, due to the lack of MHC I that is shown to the T Cells. In other words: the immune system is unable to track down these tumor cells. So it is crucial to understand MHC I development and regulation in order to fight the development of tumor cells. The Boes laboratory studies the regulation of the MHC-I gene in neuroblastoma to enhance its potential for therapeutic T-cell targeting.
At the contact site where antigen and T cells meet, specific signals trigger the adaptive immune response. From genetic screening of patients with immunodeficiencies, we identify mutations in proteins that are involved with immune cell function. One example is PSTPIP1, a protein that regulates how molecules are presented at the cell surface, so they can interact with their counterparts on other cells to build immune responses.
We study mechanisms that cause long-lasting inflammation, such as in psoriasis that mainly affects the skin. Up to 30% of psoriasis patients develop musculoskeletal inflammation, termed psoriatic arthritis. We studied how variation in CD155/DNAM1/TIGIT expression levels under inflammatory conditions may lead to altered interactions at the APC-T cell contact site. Our studies offer potential targets for immunotherapy to apply in autoimmune disease and cancer (to reduce or increase the immune response, respectively).