Claudia Kemper, PhD.PULMONOLOGY, AMD AND PNH SCIENTIFIC ADVISORY BOARD
Professor of Innate Immunology, King’s College London, UK
Dr. Claudia Kemper moved into the world of complement while conducting her PhD thesis work at the Bernhard-Nocht-Institute for Tropical Medicine in Hamburg and the Texas University, IMM, Texas, USA. Her thesis work sparked her interest in the role of complement in immunological and inflammatory processes. Dr. Kemper made her way into the innate immunity of mice and men when she joined the laboratory of John Atkinson at Washington University in Saint Louis in 1999 as a postdoctoral fellow. Dr. Kemper joined the faculty of Washington University in 2004 as instructor and became a Research Assistant Professor in 2006, continuing to further analyze the biology of CD46-activated T cells as her major research interest. Dr. Kemper was recruited into the faculty of King’s College in London, MRC Centre for Transplantation in 2008 where she now works as a Reader and focuses on the complement-mediated regulation of human effector T cell responses.
Although her group has a strong emphasis on basic scientific research, through fruitful ongoing collaborations with several clinical groups, the Kemper laboratory is applying their research towards the design of new therapeutic strategies to alter the activity of T cells as needed in cases such as autoimmunity, chronic pathogen infections or transplant rejection. The complement system rapidly recognizes and destroys invading pathogens and other harmful entities. It was long thought to be a primitive “stop-gap” measure used to slow down infection until the more sophisticated adaptive immune system can undertake its highly potent attacks using antibodies and cells tailored to the specific target. It has become clear how simplified this view had been: the successful immune defense is now seen as a complex process in which complement plays vital roles in instructing and guiding the adaptive response. Her laboratory focuses on how this communication is achieved.