Abstract
Neonatal injection of BALB/c mice with antibodies specific for the idiotype of TEPC‐15 myeloma protein (T15id), which is serologically identical to the major idiotype of anti‐phosphorylcholine (PC) antibody, renders the recipients completely unresponsive to PC. C57BL/6, (BALB/c × C57BL/6)F1 and C.B20 mice, similarly treated with anti‐T15id antibody, also displayed tolerance to PC although they were relatively more resistant (8–13%) than BALB/c mice (<2% control response). When anti‐T15id antibody was injected into 15‐day‐old neonates, the resistance to the tolerance in C57BL/6 and C.B20 mice was much more apparent (up to 80% of the control response) in contrast to that in BALB/c mice, which was not significant. Adoptive transfer of spleen cells from idiotypically suppressed BALB/c mice into 20‐day‐old normal C.B20 mice resulted in suppression of T15id but not in tolerance to PC, due to increased production of non‐T15id‐bearing anti‐PC antibody. These results suggest that the ability of clonal compensation for T15id suppression is acquired during early life (2–10 days), under the influence of gene(s) associated or linked with the Igh.