Professor of Transplant Immunology
The activation of T cells is a critical part of the immune response. Without effective T cell responses we could not fight off infections properly and vaccines would not work. However, T cell responses can also be dangerous to our bodies and it is clear that diseases such as rheumatoid arthritis and type-I diabetes as well as rejection of transplanted organs all involve unwanted T cell responses.
My laboratory works on fundamental aspects of how T cells determine whether to make immune responses or not. In particular we focus on the interplay between two receptors on T cells, CD28 and CTLA-4 and their binding partners, CD80 and CD86. Our work on the underlying molecular and cellular mechanisms has led to advances in understanding how the CD28/CTLA-4 system functions and this knowledge has been used to develop tests of human T cell function and regulatory T cell suppression.
We work closely with clinical colleagues performing research aimed at identifying gene mutations that cause immune dysregulation. This involves primary immune deficiencies, where we have worked on understanding CTLA-4 deficiency. Using blood cells from patients and unique experimental approaches we have identified regulatory T cell defects in CTLA-4-deficient patients. We are also interested in developing functional approaches to study more complex (auto)immune problems, for example in disorders such as arthritis and transplant rejection.