Studies on the Runting Syndrome in Newborn Mice* by Gregory

I t was found by BiUingham and Brent (1), by Simonsen (2), and by Woodruff and Sparrow (3) that a considerable percentage of newborn mice, rats, and chicks which were treated with adult, homologous spleen cells, lymph node ceils, buffy coat leucocytes (4), or thymus ceils (4), after an initial period of apparently normal growth, became ill, exhibited a failure to grow at a normal rate, and died by 4 weeks of age. This disease has been referred to as the runting syndrome. I t has been reported that runted mice exhibit diarrhea (3, 4), an anemia with a positive Coombs test (2), splenomegaly (2, 5, 6), hepatomegaly (5, 6), and atrophic changes of their lymphoid tissue (1, 2, 4, 7). Billingham and his coworkers found that the incidence of mating in mice varied with different strain combinations (4), being greater with greater genetic disparity between donor and recipient (4). They also found that the rtmted mice were tolerant of skin grafts from the original cell donor's strain (1, 4). Simonsen (2) found that blood from adult chicks produced splenic enlargement if given to chick embryos, while blood from newborn chicks was not active. Mechanical disruption of the cells in a Potter homogenizer destroyed their spleen-enlarging activity (2). Inoculation of parent strain newborn mice or chicks with spleen cells from the F 1 hybrid of that strain with some other strain failed to produce runting (4-5); while parent strain spleen cells produced mating of newborn F 1 hybrid animals (5). Most workers in the field (1, 2) have considered the mating syndrome to be the result of an immunological reaction of the grafted spleen cells against a tolerant host. I t is the purpose of this paper to explore further certain aspects of the runting syndrome, including several immunological methods for protecting newborn mice against the development of the syndrome.