Abstract
RECENTLY, Simonsen1 and Siskind, Leonard and Thomas2 have reported attempts to produce ‘runt disease’ in neo-natal mice by the passage of the cellular chimera established in lymphoid organs of infant mice following the injection of spleen cells obtained from adult mice. As Simonsen and Jensen3 had previously noted that splenic enlargement was a regular and early symptom in affected animals, this phenomenon was used by Simonsen to assess the graft-versus-host response. He concluded that the chimeric cells fail to produce runt disease on passage. This finding appears to conflict with the results described by Siskind and his colleagues, who observed that infant recipients of the appropriate strain not only showed similar symptoms on passage of the chimeric cells, but also that the runt syndrome observed in the passage animals was symptomatically more severe. The analysis of the runt syndrome carried out in this Laboratory supports and extends the findings described by Simonsen.
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References
Simonsen, M., Ann. N.Y. Acad. Sci., 87, 382 (1960).
Siskind, G., Leonard, L., and Thomas, L., Ann. N.Y. Acad. Sci., 87, 452 (1960).
Simonsen, M., and Jensen, E., in Biological Problems of Grafting, edit. by Albert, F., and Medawar, P. B. (Blackwell Scientific Publications, Ltd., Oxford, 1959).
Billingham, R. E., and Brent, L., Phil. Trans. Roy. Soc., B, 242, 439 (1959).
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DINEEN, J. Acquisition of Graft versus Host Tolerance. Nature 189, 680–681 (1961). https://doi.org/10.1038/189680a0
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DOI: https://doi.org/10.1038/189680a0
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