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[Prevention and treatment of acute graft-versus host disease]
1Centre Régional de Transfusion Sanguine, Besançon.
Graft-versus host disease (GvHD) is a major and at times lethal complication of allogeneic bone marrow transplantation, particularly in case of genetic disparity. Although T-cell depletion of the marrow graft is the most effective prophylaxis, its use is controverted because of the role it plays in the increase of failed transplantations and leukaemia relapses, but the overall survival rate remains unchanged. The fact that patients without GvHD have a much better quality of life justifies the current clinical research on partial or selective T-cell depletion, aimed at reducing the GvHD effect while preserving the antileukaemic effect. Biological response modifiers (haemotopoietic growth factors, lymphokins, monoclonal antibodies) are recent tools issued from biotechnology, which can act at 3 levels in the prevention and treatment of GvHD: they can reduce the undesirable effects of T-cell depletion, intervene in the antileukaemic reaction and act on GvHD effectors.
Graft-versus host disease (GvHD) is a major and at times lethal complication of allogeneic bone marrow transplantation, particularly in case of genetic disparity. Although T-cell depletion of the marrow graft is the most effective prophylaxis, its use is controverted because of the role it plays in the increase of failed transplantations and leukaemia relapses, but the overall survival rate remains unchanged. The fact that patients without GvHD have a much better quality of life justifies the current clinical research on partial or selective T-cell depletion, aimed at reducing the GvHD effect while preserving the antileukaemic effect. Biological response modifiers (haemotopoietic growth factors, lymphokins, monoclonal antibodies) are recent tools issued from biotechnology, which can act at 3 levels in the prevention and treatment of GvHD: they can reduce the undesirable effects of T-cell depletion, intervene in the antileukaemic reaction and act on GvHD effectors.