Allogeneic bone marrow transplantation (BMT) is an effective curative therapy for the majority of haematological malignancies and severe immunodeficiencies. The therapeutic potential of this procedure arises from the graft-versus- leukaemia (GVL) effect, which eradicates recipient malignancy after BMT and is mediated by donor T and natural killer (NK) cells. Unfortunately, GVL effects are inextricably linked to graft-versus-host disease (GVHD), the major cause of transplant-related mortality. GVHD manifests in two forms; acute and chronic GVHD. During acute GVHD, the skin, gastrointestinal tract, and liver are preferentially damaged by the transplanted donor immune system. Chronic GVHD generally develops in the later phase after transplant characterised by end-organ fibrosis. In the early stages of GVHD, donor T cells react to recipient- derived alloantigens presented predominantly by recipient antigen-presenting cells (APCs). Additionally, the success of transplant outcome is also determined by the potential for graft failure due to responses against donor immunohaematopoietic cells by recipient T or NK cells. Thus, there remains a clear need for greater understanding of the factors which lead to GVHD, associated opportunistic infection and disease relapse. Ultimately the aim is to reduce GVHD and associated immune deficiency whilst promoting the immunological clearance of leukaemia.