Origins of peripheral B cells in IL-7 receptor-deficient mice

David G.T. Hesslein, Shu Yuan Yang, David G. Schatz*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

20 Scopus citations


The interleukin 7 (IL-7) signaling pathway is critical for early lymphoid differentiation. We found dramatic perturbations in fetal liver B cell development and confirmed a complete absence of developing B cells in the adult bone marrow in mice lacking the IL-7 receptor alpha (IL-7Rα) gene. We show that peripheral B-2 and B-1 cell populations are deficient in IL-7Rα-/- mice. B-2 follicular cell and peritoneal B-1 cell percentages are reduced, while B-2 marginal zone cell percentages are increased. A comparison of bone marrow and splenic populations at different ages revealed that the splenic B cell populations seen in adult IL-7Rα-/- mice first appear during neonatal development. We have measured N-nucleotide addition at the joints of V(D)J rearrangements in splenic B cells and have used it as a somatic marker to define and separate bone marrow-derived B cells from fetal liver-derived B cells. B cells isolated from the bone marrow and spleen of adult and neonatal IL-7Rα-deficient mice harbor high levels of N-nucleotide additions similar to those found in equivalent wild-type B cell populations. We conclude that the majority of splenic B cells in IL-7Rα-deficient mice originate from the bone marrow and not the fetal liver.

Original languageEnglish
Pages (from-to)326-334
Number of pages9
JournalMolecular Immunology
Issue number4
StatePublished - 02 2006
Externally publishedYes


  • Antibodies
  • B lymphocytes
  • Cytokine receptors
  • Gene rearrangement
  • Hematopoiesis


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