The graft versus host reaction (GVH) remains the major setback of allogeneic bone marrow transplantation. GVH is observed in more than 50% of HLA identical transplantations. GVH can occur as an acute or chronic syndrome. The severity is variable, the GVH being responsible for the death of 10 to 20% of transplanted patients. Cytotoxic T lymphocytes or helper T lymphocytes are able on their own to mediate the GVH reaction. These T lymphocytes are specific for minor histocompatibility antigens. Some of them are restricted to specific tissues such as the skin. The frequency of the GVH reactions is increasing with the age of the recipient, with the degree of HLA antigens incompatibility and with presence of viral infections in the host. Several ways of GVH reaction prevention have been used such as the use of Methotrexate or Cyclosporin A. T cell depletion of the bone marrow appears to be the most effective method, allowing the achievement of HLA mismatched bone marrow transplantation. However, bone marrow T cell depletion is associated in 10 to 20% of cases with graft failure. The rate of graft failure is extremely high for HLA incompatible bone marrow transplantations. This could be due to the lack of antirejection effect of donor T lymphocytes. Graft rejection is mediated by host residual immunity. Cytotoxic T lymphocytes and perhaps natural killer cells are the effector cells. Several procedures attempting at the prevention of graft failure are currently under investigation. They tend to block the host residual immunity either by increasing chemotherapy or total irradiation, by using lymphoid irradiation or by the in vivo infusion of monoclonal antibodies specific for lymphoid cells.