Bcl11a is essential for normal lymphoid development

Pentao Liu, Jonathan R. Keller, Mariaestela Ortiz, Lino Tessarollo, Rivka A. Rachel, Takuro Nakamura, Nancy A. Jenkins, Neal G. Copeland

Research output: Contribution to journalArticlepeer-review

241 Scopus citations


Bcl11a (also called Evi9) functions as a myeloid or B cell proto-oncogene in mice and humans, respectively. Here we show that Bcl11a is essential for postnatal development and normal lymphopoiesis. Bcl11a mutant embryos lack B cells and have alterations in several types of T cells. Phenotypic and expression studies show that Bcl11 a functions upstream of the transcription factors Ebf1 and Pax5 in the B cell pathway. Transplantation studies show that these defects in Bcl11a mutant mice are intrinsic to fetal liver precursor cells. Mice transplanted with Bcl11a-deficient cells died from T cell leukemia derived from the host. Thus, Bcl11a may also function as a non-autonomous T cell tumor suppressor gene.

Original languageEnglish (US)
Pages (from-to)525-532
Number of pages8
JournalNature immunology
Issue number6
StatePublished - Jun 1 2003

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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