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Department of Surgery, The Mount Sinai Hospital, New York, New York
Graft-versus-host reactions, which may occur following the inoculation of immunologically competent cells into susceptible antigenic hosts, initiate a complex immunopathologic syndrome. The most characteristic feature of this experimental disease is widespread involvement of lymphoid tissue, typified by an early proliferative phase followed by varying degrees of lymphoid depletion and atrophy. Although there is little disagreement today over the graft-versus-host etiology of runting and wasting disease, there is little insight into their pathogenesis. The similarities between the effects of graft-versus-host reactions and other experimental wasting diseases have served to emphasize the unhealthiness of lymphoid tissue depletion.
Graft-versus-host reactions have served as valuable tools for studying the population dynamics of grafted immunologically competent cells and are currently gathering increasing interest in relation to so-called autoimmune disease and lymphoproliferative disorders. An examination of the evidence relating to the fate of grafted lymphoid cells engaged in graft-versus-host reactions underscores the rather limited capacity such cells have for continuous immunologic aggressiveness. Thus it seems that currently used models of graft-versus-host reactions possess little in common with spontaneous disease states in man in which autoimmune mechanisms are thought to play a role.
1 The studies carried out in the author's laboratory have been supported in part by USPHS Grants AM-08954 and AM-10036 and by Grants U-1170, U-1546, and U-1673 from the Health Research Council of the City of New York.
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