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1.
Adult (8-week-old) SJL mice reach a relatively low degree of tolerance when injected with aggregate free rabbit γ-globulin (RGG). To analyze this phenomenon, we first examined indirect plaque-forming responses (PFC) in terms of participation of accessory and thymus-derived cells. Double transfer experiments were used; accessory cells were removed from donor cells by filtration over glasswool and their capacity reduced in recipients by 3 day preirradiation or by horse erythrocyte-mediated blockage. Using this type of experimental arrangement we found that the antibody response to RGG required the cooperation of accessory and thymus-derived cells. The induction of tolerance was affected by the presence of accessory cells. Preirradiated secondary recipients were reconstituted with spleen cells from accessory cell-deprived donors which had received thymus and bone marrow cells. In some experiments, the thymus and bone marrow cells were passed over glasswool. The primary recipients were left untreated or were given tolerogen. A more profound state of tolerance (reduction in plaque forming response) was the consequence of the incapacitation or removal of accessory cells. The magnitude of the reduction in PFC was directly related to the completeness of accessory cell removal and incapacitation. Responsiveness could be restored by administration of irradiated spleen cells as a source of accessory cells. The need for thymus-derived (T) cells in the antibody response was demonstrated by double transfer experiments in which the primary recipient was restored with thymus cells alone, bone marrow cells alone, or with a mixture of cell types.  相似文献   

2.
The half-lives of elimination (T12) of 131I-RGG from the body of normal A or Balb/c animals was much longer than the T12 of SJL mice. At all ages, the T12 of normal hybrids (A × SJL, SJL × A, Balb/c × SJL) was similar to or longer than that of the A or Balb/c parents. Thus, in terms of the T12 of normal animals, the SJL responsiveness to 131I-RGG appeared to be a recessive trait. Tolerance could be induced in newborn animals and, in terms of T12, the degree of unresponsiveness at the age of 6 weeks, was the same in A, Balb/c, A × SJL, and Balb/c × SJL animals but was much shorter in SJL mice. Thus, in neonatally induced tolerance, the duration of tolerance was recessive for the SJL type. The average Tbuilt12 after tolerance induction in 3-week-old hybrids (A × SJL, SJL × A, Balb/c × SJL) was similar to that of the A or Balb/c parent, but by the 8th and 12th week it approached the average T12 of the SJL parent. Comparing 8-week-old hybrids, the average T12 was longest in A × SJL hybrids and identical in SJL × A and Balb/c × SJL mice. An examination of T12 distribution in various 8- and 12-week-old crosses and backcrosses revealed a fairly large proportion of individuals with a T12 which was intermediate between SJL and the other parent. There was a tendency for this number to decrease in 12 weeks as compared to 8-week-old mice. In 8-week-old mice, the number of animals with intermediate Tbuilt12 was smallest when SJL was the maternal animal [(SJL × A); SJL × (A × SJL); SJL × (SJL × A)]. There was no link between T12 of tolerant animals and either the immunoglobulin allotype (MuAl/MuA2) or the C5 eniotype (MuB1 positive/MuB1 negative).  相似文献   

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