Our immune system is made up of billions of immune cells called lymphocytes. These cells are continuously being produced in the bone marrow (B lymphocytes) and thymus (T lymphocytes) and circulate through our bodies until most commonly they die from neglect or ageing. Each lymphocyte expresses a unique receptor that enables it to detect a specific set of molecules termed antigens. By chance some lymphocytes have receptors for foreign antigens that are unique parts of the molecular makeup of infectious organisms. When these rare lymphocytes bind a foreign antigen during an infection, they receive a signal to multiply and then destroy the infectious agent; and when some of the antigen specific cells persist they provide an "immunological memory", which is what happens when we are immunised. The generation of lymphocyte receptors is done at random because otherwise the infectious agents would find a way to develop resistance, just as they do in response to antibiotics. However, because the process is random, it is inevitable that sometimes lymphocytes will carry receptors for self-antigens - in other words, they will react with molecules in our own bodies.
Our aim is to understand how this process normally occurs and how it is controlled to prevent "friendly fire". We want to understand what happens when control breaks down, in autoimmune diseases, such as insulin dependent diabetes mellitus (caused by lymphocytes attacking the insulin producing cells of the pancreas) or rheumatoid arthritis (caused by lymphocytes attacking the cartilage of the joints). We are discovering why some people are susceptible to these diseases, and conversely why some people are unable to respond at all, and we are using our knowledge to design new treatments.