So GvHD is a clinical manifestation of the allo-reactivity of donor T-cells against antigens in the patient that are different from those of the donor. Those could be HLA antigens in the case of HLA mismatch transplants. Or they could be minor histocompatibility antigens, which are just normal variations in proteins that have a slightly different gene sequence across the population. We know that the risk of graft-versus-host disease increases significantly when GvHD prophylaxis is eliminated as part of the transplant maneuver...
So GvHD is a clinical manifestation of the allo-reactivity of donor T-cells against antigens in the patient that are different from those of the donor. Those could be HLA antigens in the case of HLA mismatch transplants. Or they could be minor histocompatibility antigens, which are just normal variations in proteins that have a slightly different gene sequence across the population. We know that the risk of graft-versus-host disease increases significantly when GvHD prophylaxis is eliminated as part of the transplant maneuver. However, by manipulating the content of T-cells in the graft and by giving the appropriate pharmacological inhibitors, we can manage the risk of graft-versus-host disease so that patients will have the benefit of the graft-versus-leukemia effect without life threatening graft-versus-host disease complications.
