Feedback regulation of murine Ly-1 B cell development

Eur J Immunol. 1989 Mar;19(3):507-13. doi: 10.1002/eji.1830190315.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Animals, Newborn / immunology
  • Antibodies, Anti-Idiotypic / immunology
  • Antigens, Ly / analysis*
  • B-Lymphocytes / physiology*
  • Cell Separation
  • Feedback
  • Hematopoietic Stem Cells / immunology
  • Immunization, Passive
  • Immunoglobulin Allotypes / immunology
  • Immunoglobulin M / immunology
  • Immunoglobulin M / metabolism
  • Immunoglobulins / analysis
  • Mice


  • Antibodies, Anti-Idiotypic
  • Antigens, Ly
  • Immunoglobulin Allotypes
  • Immunoglobulin M
  • Immunoglobulins