title: Feedback regulation of murine Ly-1 B cell development.
abstract: Studies 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. The 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 influence Ly-1 B development during neonatal life.
authors: Department of Genetics, Standford University, CA 94305.
authors: P A
authors: PA
authors: Lalor
authors: L A
authors: LA
authors: Herzenberg
authors: S
authors: S
authors: Adams
authors: A M
authors: AM
authors: Stall
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000276:immunology; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000950:Antigens, Ly / Q000032:analysis*; D001402:B-Lymphocytes / Q000502:physiology*; D002469:Cell Separation; D005246:Feedback; D006412:Hematopoietic Stem Cells / Q000276:immunology; D007116:Immunization, Passive; D007126:Immunoglobulin Allotypes / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology / Q000378:metabolism; D007136:Immunoglobulins / Q000032:analysis; D051379:Mice
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000950:Antigens, Ly; D007126:Immunoglobulin Allotypes; D007075:Immunoglobulin M; D007136:Immunoglobulins