Abstract

SummaryWhen lethally-irradiated CBA.T6T6 mice were grafted with mixtures of C57BL and (C57BL × CBA.T6T6)F1 cells of bone-marrow or foetal liver the incidence of secondary disease was considerably reduced as compared with mice receiving the incompatible C57BL cells only. Cytogenetic examination of bone-marrow, spleen, thymus and lymph node and identification of CFU in blood showed that F1 cells were not eliminated as anticipated and that C57BL cells persisted in similar numbers, whether or not the host had secondary disease. The mechanism of avoidance of secondary disease in these experiments appears to be adaptation of the incompatible allogeneic graft, the host being carried through the periods of haemopoietic and immunological insufficiency by the F1 cells. The findings constitute not only a therapeutic advance in a hitherto incompatible graft-versus-host relationship but also require reappraisal of the dominant role accorded to GVHR in secondary disease.

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