DISCUSSION 269 



HiUemann: We had no tolerant survivors at all. I should add that we 

 had no evidence of immunity in these animals either ; thus the A-hne 

 recipients were not immunized as a consequence of their exposure to 

 C57BL small lymphocytes and subsequent recovery from runt disease. 

 The median survival times were right in the middle of the usual range. 



Billingham: Dr. Silvers and I have been using the CBA to A mouse 

 strain combination to compare the abihty of cells o£ different histological 

 origins to confer tolerance when inoculated intravenously into neo- 

 natal hosts. As might be expected, cell suspensions prepared from nodes 

 and spleens caused runt disease in many of the subjects, with variable 

 mortaHty, Nearly all the animals which survived the injection of i or 

 2 milhon node cells proved to be tolerant of CBA skin. Homologous 

 marrow and spleen cells provided much less effective tolerance-con- 

 ferring stimuH than node cells, though they caused less runt disease. 



To eliminate the occurrence of runt disease, (CBA x A) F^ cells were 

 employed. To our considerable surprise F^ hybrid axillary and brachial 

 node cells proved to be a highly inefficient tolerance-conferring stimulus 

 — inferior in fact to adult thymus cells. Similar findings have been 

 obtained in experiments with rats. One possible explanation for the 

 wide disparity in results obtained with F^ hybrid node cells on the one 

 hand and with parental-strain node cells on the other is that the latter 

 are stimulated to proHferate and increase their dosage after inoculation 

 by the antigenic stimulus of their hosts. Some evidence in support of 

 this interpretation comes from the fact that increasing the dosage of 

 F^ lymphoid cells in rats to a relatively high level does result in the in- 

 duction of tolerance of subsequent skin homografts. 



HiUemann: If the small lymphocytes that we are injecting are cap- 

 able of transforming to other cells in large numbers, namely pyronino- 

 philic cells or "haemocytoblasts", then why should these A-line mice 

 not have become tolerant of C57 antigens ? If, on the other hand, these 

 cells are mostly end cells (which our tritiated thymidine evidence in- 

 dicates), then the results would stand as I have interpreted them. I 

 agree with Dr. Brent that a small proportion of C57 cells might have 

 been present but not detected in the A-Hne survivors. The reason for 

 this is that in teasing the cells from the lymph nodes you always damage 

 some, so the cell control tubes (lacking antiserum) always show a low 

 proportion of stained cells. The number of stained cells from A-line 



