AbstractStudies presented here, conducted with allotype homozygotes, demonstrate the existence of a feedback mechanism that regulates development of Ly‐1 B cells from immature progenitors. In the preceding study (P. A. Lalor et al.,Eur. J. Immunol.1989.19: 501), conducted with allotype heterozygotes, we showed that treating neonates with monoclonal antibody to the paternal allotype IgM depletes roughly half of the neonatal B cell population (i.e.those expressing the paternal IgM allotype) and that paternal allotype Ly‐1 B cells specificically remain depleted for the life of the animal. Here we show that treating allotype homozygotes with the same antibody depletes all (rather than half) of the B cells and that, under these conditions, relatively normal numbers of Ly‐1 B cells reappear shortly after the treatment antibody disappears. This recovery, we also show, is prevented by restoring allotype‐congenic Ly‐1 B cells to the treated homozygotes,i.e.by reconstituting treated neonates with allotype‐congenic peritoneal cells, sorted Ly‐1 B cells or a monoclonal population of Ly‐1 B “tumor” cells.These findings in essence reveal a feedback mechanism through which mature Ly‐1 B cells prevent further Ly‐1 B cell development from Ig‐precursors. This feedback regulation is independent of Ig secretion by the mature Ly‐1 B cells, since the monoclonal Ly‐1 B “tumor” population that prevents endogenous Ly‐1 B development does not secrete Ig. Furthermore, it appears to be independent of Ly‐1 B surface Ig specificity, since a monoclonal population is sufficient to block all Ly‐1 B cell development. This mechanism appears to operate normally to fix the composition of the Ly‐1 B population, which survives through self‐replenishment in adults, in accord with conditions that influe
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