Autologous graft-vs host disease: Mechanism and potential therapeutic effect

A. D. Hess, R. C. Jones, G. W. Santos

Research output: Contribution to journalArticlepeer-review

Abstract

Administration of the immunosuppressive drug cyclosporine (CsA) after autologous or syngeneic bone marrow transplantation (BMT) elicits an autoimmune syndrome with pathology identical to graft-vs-host disease (GVHD). This syndrome can be induced both in man and in rats and is associated with the development of cytolytic autoreactive T cells that recognize MHC class II determinants. Studies in a rat model suggest that there are two essential components necessary for the induction of an autologous/syngeneic GVHD and include the inhibition of thymic dependent clonal deletion of autoreactive T lymphocytes by CsA and the elimination of a peripheral regulatory mechanism by the preparative regimen. The absence of peripheral autoregulation creates a permissive environment for the activation of the autoreactive T cells. Based on on understanding of the immunobiology of this autoimmune syndrome, we have utilized the induction of autolegous/syngeneic GVHD in an attempt to provide an antitumor therapeutic effect after autologous BMT. Interim analyses of our clinical trials suggest that this approach is quite promising.

Original languageEnglish (US)
Pages (from-to)S65-S69
JournalBone marrow transplantation
Volume12
Issue numberSUPPL. 3
StatePublished - 1993

ASJC Scopus subject areas

  • Hematology
  • Transplantation

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