Studies on the Mechanism of Secondary Disease The Parental-F 1 Hybrid Radiation Chimera

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Abstract
A lethal wasting syndrome is elicited, in sublethally X-irradiated (500 r) LAF1 hybrids, not only when A-strain spleen cells (25x10) are injected immediately after irradiation, but also after an interval of 8, 15, or 22 days postirradiation. Apparently, functional lymphoid recovery has not as yet occurred at this time in spite of recovery of spleen cellularity by 22 days. At 35 and 47 days after 500 r, the F1 hybrids survive after injection of spleen cells. Injection of A-strain spleen cells into nonirradiated LAF1 young adult recipients (9 to 15 weeks of age) does not elicit death; by contrast, administration of A-strain spleen cells into nonirradiated old LAF1 mice elicits deaths, with concomitant histological evidence of lymphoid tissue degeneration. A mechanism for the lethal syndrome is proposed. 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 of both donor and host lymphoid cells, and in an animal with atrophic lymphoid tissues. The hypothesis accounts for the differential in lymphoid regeneration in lethally X-irradiated recipients after isologous marrow therapy. Deaths in the old nonirradiated LAF1 mice injected with A-strain spleen cells is attributed to a relatively deficient lymphoid tissue regenerative potential, as compared to that of young adult mice.

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