Abstract
The wasting syndrome was elicited in 500 r x-irradiated LAf/sub 1/ hybrid mice, not only when A-strain spleen cells were injected immediately after irradiation, but also after an interval of 8, 15, or 22 days postirradiation. Apparently, functional lymphoid recovery had not as yet occurred at this time, in spite of the spleen weight recovery after 15 days. At 47 days post 500 r, the Ft hybrids were able to survive after infection of spleen cells. In non-irradiated LAf/sub 1/ mice, injection of A-strain spleen cells into young adult recipients did not elicit deaths; by contrast, injection of A spleen cells in non-irradiated old LAf/sub 1/ mice caused deaths. On the basis of these findings, a mechanism of production of the lethal syndrome is proposed, and some consequences with respect to the general problem of secondary disease are discussed. It is suggested that secondary disease involves a continuous dynamic, mutual cell-to- cell homograft reaction between donor and host lymphoid cells, which results in killing off of both types of lymphoid cells, and an animal with atrophic lymphoid tissues. The hypothesis also accounts for the differential in lymphoid regeneration in lethally x-irradiated recipients following isologous versus non- isologous marrow therapy. (auth)
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