Graft versus host inhibition. iii. fetal thymic factor and fetal liver cells to minimize secondary disease.

TLDR: It was concluded that the strain A fetal liver-thymus combinations acted synergistically to enhance survival of the CBA mice, probably caused by a subcellular factor from the fetal thymus which acted on the liver cells.

Abstract: SUMMARY Lethally irradiated CBA host mice were given i.v. injections of perinatal liver hematopoietic cells from strain A donors. Survival studies demonstrated that 57% of the hosts were alive at 100 days when treated with fetal liver cells, and 50% survived 100 days when treated with liver cells from 5-day-old mice. All lethally irradiated CBA mice survived 100 days when protected with strain A fetal liver cells i.v. plus i.p. Millipore chambers containing thymus cell suspensions from strain A fetal donors. This salutary effect on survival, over that observed with liver cells alone, was highly significant (P < 0.001). This beneficial effect on survival was eliminated when the Millipore chambers containing fetal thymus tissue were first stored 8-10 days in temporary syngeneic hosts. The addition of thymus tissue in Millipore chambers from strain A 5-day-old donors did not significantly alter survival from that observed when only liver cells were given. It was concluded that the strain A fetal liver-thymus combinations acted synergistically to enhance survival of the CBA mice. This effect was probably caused by a subcellular factor from the fetal thymus which acted on the liver cells. It was noteworthy that the subcellular factor was apparently present only in the fetal thymic tissue. Secondary disease was at a minimum as evidenced by the excellent long-term survival, healthy and vigorous appearance of the mice, absence of overt graft-versus-host disease, and absence of overt infection.