The Journal of Experimental Medicine
Avanti Polar Lipids
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© The Rockefeller University Press, 0022-1007/2000/1/23/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 1, January 3, 2000 23-32


Original Article

Precursor B Cell Receptor–dependent B Cell Proliferation and Differentiation Does Not Require the Bone Marrow or Fetal Liver Environment

Antonius G. Rolinka, Thomas Winklerb, Fritz Melchersa, and Jan Anderssona
a Basel Institute for Immunology, CH-4005 Basel, Switzerland
b Department of Immunology, Friedrich-Alexander University, D-91054 Erlangen, Germany

Correspondence to: Antonius G. Rolink, Basel Institute for Immunology, Grenzacherstrasse 487, CH-4005 Basel, Switzerland. Tel:41-61-605-1265 Fax:41-61-605-1364 E-mail:rolink{at}bii.ch.

The capacity of precursor B (pre-B) I cells from fetal liver and bone marrow to proliferate and differentiate into surface immunoglobulin–positive immature B cells in vitro was analyzed. Both fetal liver– and bone marrow–derived progenitors do so in a pre-B cell receptor (pre-BCR)–dependent manner in tissue culture medium alone, without addition of other cells or cytokines. Approximately 20% of the initial pre-B I cells enter more than one division. Analyses at the single-cell level show that ~15% divide two to five times. Coculture of pre-B I cells with stromal cells did not enhance proliferation or differentiation, whereas the presence of interleukin 7, especially in combination with stromal cells, resulted mainly in the expansion of pre-B I cells and prevented their further differentiation. Thus, the environment of fetal liver or bone marrow is not required for the pre-BCR to exert its function, which is to select and expand cells that have undergone an inframe VH-DHJH rearrangement that produces a pre-BCR–compatible µH chain. It appears unlikely that a ligand for the pre-BCR drives this pre-B cell proliferation.

Key Words: B cell development, precursor B cell receptor, {lambda}5, c-kit, bcl-2


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