Research in the Thymus Biology Unit initially focused on cloning and characterising different subsets of T-cells. It used tools such as antigen markers, release factors, aspects of MHC restriction and alloreactivity against foreign MHC components within the same species. Within a year, the work concentrated heavily on the mechanisms by which T-lymphocytes recognise antigen. By 1987/88 the Unit's focus had been refined to researching T-cell receptor gene expression in T-cell subsets. They looked at the role of accessory molecules in T-cell activation and self-tolerance by first examining the idea of clonal deletion of self-reactive T-cells in the thymus. The Unit extended this study to post-thymic tolerisation from 1989/90, primarily using transgenic mouse models.

In 1990/91 the Thymus Biology Unit began studying the role of MHC class II genes in protecting NOD (non-obese diabetic) mice from developing insulin-dependent diabetes mellitus (IDDM) and the search for 'faulty' tolerance genes, such as those connected to autoimmune diabetes. Research into how T-lymphocytes sometimes react against the body's own tissues and cause autoimmune diseases such as diabetes, rheumatoid arthritis or multiple sclerosis continued until 1995/96. That same year the Unit became the first to successfully map a gene involved in 'preclinical' diabetes: the gene IDDM13 that predisposes people to insulin-dependent diabetes.