T-cells are activated when they recognise foreign antigens or pathogenic self-antigens. These antigens are “seen” by the T-cell through the T cell receptor (TCR) and have been processed and subsequently displayed on other cells through the major histocompatibility complex (MHC) molecule. However, the ultimate outcome of T-cell activation also depends on many other factors, including the binding strengths of the antigen to MHC or to the TCR, the presence of coreceptors on the T-cell (CD4 and CD8), as well as the engagement of other co-stimulatory molecules (such as CD28 and B7). I am interested in studying how TCR engagement to the MHC molecule (presenting the antigen) affects the resulting effector functions of T-cells. One of my current projects involve examining how TCR affinity impacts on T-cell function. The significance of this work is to ultimately decipher the degree of antigen affinity required to tailor the TCR in order to achieve an optimal protective immune responses in specific diseases.