p53 regulates Btk-dependent B cell proliferation but not differentiation

Nathan W. Schmidt, Lindsey D. Mayo, David B. Donner, Mark H. Kaplan

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

Btk is critical for B cell development and proliferation. Mice lacking Btk have a defect in B cell development, resulting in a loss of mature B cells and decreased proliferative responses following B cell receptor cross-linking. In contrast, mice deficient in the tumor suppressor p53 display increases in developing B cell populations in the bone marrow. To investigate the potential role of p53 in Btk-dependent B cell development and function, we generated mice doubly-deficient in p53 and Btk. Btk/p53-deficient mice showed an increase in splenic B220+ cell numbers compared with Btk-deficient mice, although there was no recovery in B cell subset differentiation. In contrast to the lack of recovery of B cell development, there was a recovery in lipopolysaccharide and anti-immunoglobulin M (IgM) plus interleukin-4-induced proliferation of Btk/p53-deficient B cells, although there was no recovery to anti-IgM stimulation alone. Thus, p53 promotes B cell expansion and proliferation, but p53 deficiency cannot compensate for Btk deficiency in the development of B cell subsets.

Original languageEnglish (US)
Pages (from-to)852-859
Number of pages8
JournalJournal of Leukocyte Biology
Volume79
Issue number4
DOIs
StatePublished - Apr 1 2006

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Keywords

  • B lymphocyte
  • Development
  • Immunoglobulin
  • Tumor suppressor

ASJC Scopus subject areas

  • Cell Biology

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