STUDIES ON THE RUNTING SYNDROME IN NEWBORN MICE

Runting was produced by homologous spleen or lymph node cell suspensions, but not by isologous spleen or homologous liver or kidney cell suspensions. The incidence of runting (a) varied with the particular strain combination employed, (b) increased with increased dose of foreign cells, and (c) decreased as the time interval between birth and inoculation with foreign cells was increased. A focal, coagulative necrotic, liver lesion was described in runted mice. It was found that viable cells were required to produce the runting syndrome. Frozen-thawed cells, homogenized cells, and the cell-free supernatant of ground spleen suspensions failed to produce runting. Runted mice were found to have an anemia of variable degree, and white blood cell counts ranging from marked leukopenia to severe leucocytosis. Mice receiving isologous spleen or homologous liver or kidney showed normal red and white blood cell counts. Isologous spleen cells, given to newborn mice within 30 minutes following injection of homologous spleen cells, conferred significant protection against the runting syndrome. Isologous spleen injected 1 day after the injection of homologous spleen failed to protect. Newborn mice which had received homologous spleen cells were protected from becoming runted by treatment with "anti-cell donor strain" serum. The offspring of mothers which had been immunized against the spleen cell donor's strain failed to become runted when treated with homologous spleen cells. The data are regarded as compatible with the concept, presented by previous workers, that runting is the result of an immunological reaction of foreign cells against a tolerant host.