Impaired granulopoiesis, myelodysplasia, and early lethality in CCAAT/enhancer binding protein epsilon-deficient mice

Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13187-92. doi: 10.1073/pnas.94.24.13187.

Abstract

Polymorphonuclear leukocytes are essential for host defense to infectious diseases. CCAAT/enhancer binding protein epsilon (C/EBP epsilon) is preferentially expressed in granulocytes and lymphoid cells. Mice with a null mutation in C/EBP epsilon develop normally and are fertile but fail to generate functional neutrophils and eosinophils. Opportunistic infections and tissue destruction lead to death by 3-5 months of age. Furthermore, end-stage mice develop myelodysplasia, characterized by proliferation of atypical granulocytes that efface the bone marrow and result in severe tissue destruction. Thus, C/EBP epsilon is essential for terminal differentiation and functional maturation of committed granulocyte progenitor cells.

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Proteins
  • Cytokines / genetics
  • DNA-Binding Proteins / genetics*
  • Genes, Lethal
  • Granulocytes / cytology*
  • Hematopoiesis / genetics*
  • Hematopoietic Cell Growth Factors / genetics
  • Mice
  • Mice, Mutant Strains
  • Myelodysplastic Syndromes / pathology*
  • Nuclear Proteins / genetics*
  • Recombination, Genetic

Substances

  • CCAAT-Enhancer-Binding Proteins
  • Cytokines
  • DNA-Binding Proteins
  • Hematopoietic Cell Growth Factors
  • Nuclear Proteins