Graftversushost disease

Confusion exists as to the difference between the graft-versus-host reaction and graft-versus-host disease. Graft-versus-host reaction identifies only the immunologic events that occur as a consequence of the infusion of allogeneic immunocompetent cells into a susceptible recipient. It has become apparent, especially from the studies in germ-free animals, that the clinical manifestations of the graft-versus-host reaction (graft-versus-host disease) is dependent upon many environmental factors, including the presence of endotoxin, the age of the donor and recipient, the sex of the donor, etc. Thus, strain combinations exist in which no graft-versus-host disease occurs when transplants are done between germ-free animals. However, the introduction of bacteria into the stable post-transplant chimera results in the development of clinical graft-versus-host disease, presumably secondary to the effects of endotoxin and other bacterial products/antigens. An extensive literature exists documenting the role of endotoxin in increasing the severity of graft-versus-host disease. Graft-versus-host disease is more frequently seen in the recipients of female, as opposed to male, immunocompetent cells.

Clinically, graft-versus-host disease can appear as one of two distinct forms. Acute graft-versus-host disease has its onset early following the infusion of donor immunocompetent cells and is characterized by the cytolytic destruction of the recipient epidermal cells, hepatocytes and gastrointestinal cells, producing a characteristic cutaneous erythroderma, elevation in hepatocellular enzymes and diarrhea. A high rate of fatality is found in both animals and humans with severe acute graft-versus-host disease due to the denudation of the gastrointestinal tract, epidermal sloughing, sepsis and bleeding. Individuals, who do not die from acute graft-versus-host disease, are at risk of developing chronic graft-versus-host disease, which has many similarities to autoimmune diseases, including sclerodermatous skin changes, the production of autoantibodies, etc. In model animal systems, graft-versus-host disease is usually produced by the infusion of homozygous donor immunocompetent cells into Ft recipients or of allogeneic bone marrow cells into irradiated recipients. Graft-versus-host disease can be seen following the infusion of peripheral lymphoid cells, splenocytes and bone marrow or the transplantation of lymphoid-containing organs, such as the small intestine.

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