Failure of Lymphopoiesis after Adoptive Transfer of NF-κB–Deficient Fetal Liver Cells
Abstract
Mice deficient in the p65 subunit of NF-κB die during fetal development. Introduction of p50/p65-deficient fetal liver cells into lethally irradiated hosts resulted in a severe deficit of fetal liver–derived lymphocytes and their immediate precursors but an overabundance of fetal liver–derived granulocytes. Surprisingly, simultaneous transplantation of wild-type bone marrow cells rescued the production of p50/p65-deficient lymphocytes. Expression of immunoglobulin κ light chains on these rescued NF-κB–deficient B lymphocytes was normal. These results suggest that while p50 and p65 do not regulate the maturation of pre–B cells, NF-κB mediates the development or survival of an early lymphocyte precursor through regulation of an extracellular factor.
Additional Information
© 1997 Cell Press. Under an Elsevier user license. Received 10 March 1997, Revised 23 April 1997. Correspondence should be addressed to D. B. We thank members of our laboratory for helpful discussion and comments. The S17 stromal line was kindly provided by Ken Dorshkind. Experiments involving animals were carried out under guidelines set forth by the Animal Care and Use Committee at The Massachusetts Institute of Technology. B. H. H. is supported by a fellowship from the Cancer Research Fund of the Damon Runyon-Walter Winchell Foundation. S. R. C. is supported by National Institutes of Health training grant 5 T32 GM07287. D. B. is an American Cancer Society Research Professor. Supported by a grant from the Amgen Corporation.Additional details
- Eprint ID
- 102730
- Resolver ID
- CaltechAUTHORS:20200422-150959025
- Damon Runyon Cancer Research Foundation
- 5 T32 GM07287
- NIH Predoctoral Fellowship
- American Cancer Society
- Amgen
- Created
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2020-04-23Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field