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Induction of tolerance in B-1 cells for bromelain-treated mouse red blood cells by a transient presence of anti-idiotype antibodies in neonatal and adult mice.

Murine B-1 cells are thought to develop from Ig- progenitors early in ontogeny and to expand by self-renewal. To examine the early development of Ig+ precursors of B-1 cells for bromelain-treated mouse RBC, the transient presence of RidA, a rat anti-Id mAb for V(H)11/Vkappa9-type anti-bromelain-treated mouse Abs, was produced in neonatal mice. The presence of RidA during days 0 to 10 of age resulted in an 80% reduction in peritoneal RidA-Id+ B cells and B cells secreting RidA-Id+ Ig after LPS stimulation in 8-wk-old mice. This suggests that most Ig+ precursors for adult RidA-Id+ B cells already exist in 10-d-old mice. However, RidA injected into mice on day 10 had to persist for >4 days to result in a significant reduction in adult B cells. Similarly, although RidA injected into adult mice bound immediately to membrane Ig (mIg) of the peritoneal RidA-Id+ B cells, a RidA persistence for >4 days was required to suppress LPS reactivity of peritoneal and splenic B cells. The binding of RidA to mIg preexisting on B cells has no apparent effect on the ability of neonatal B cells to expand clonally or on the ability of adult B cells to secrete RidA-Id+ Ig after LPS stimulation. Both abilities evidently are suppressed by the accumulation of reaction between freshly expressed mIg and RidA.