Cell-autonomous defects in dendritic cell populations of Ikaros mutant mice point to a developmental relationship with the lymphoid lineage

Immunity. 1997 Oct;7(4):483-92. doi: 10.1016/s1074-7613(00)80370-2.


The transcription factor Ikaros is a major determinant of lymphocyte differentiation. Mice homozygous for an Ikaros dominant-negative (DN-/-) mutation lack all cells of lymphoid origin, including T, B, and natural killer (NK) cells. Mice homozygous for an Ikaros null allele lack B and NK cells but display specific defects in T lymphocytes. Nonetheless, both Ikaros mutant lines make an excess of monocytes and macrophages. Here we report that the production of subsets of antigen-presenting dendritic cells (DCs) is also defective. By constructing bone marrow chimeras, we demonstrate that the Ikaros-mediated defect in lymphocytes and DCs is intrinsic to their precursors and is not environment dependent. The selective defects in DCs manifested with the Ikaros null mutation suggest a tight linkage between development of T cells and CD8alpha+ DCs. The complete lack of DCs in the lymphoid organs of Ikaros DN-/- micke points to an essential role for the Ikaros gene family in the development of all DCs.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bone Marrow Cells / cytology
  • CD8 Antigens / analysis
  • DNA-Binding Proteins*
  • Dendritic Cells / cytology*
  • Gene Deletion
  • Ikaros Transcription Factor
  • Leukopoiesis*
  • Lymphocyte Activation
  • Lymphocyte Subsets / cytology
  • Lymphocyte Subsets / immunology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Radiation Chimera
  • Sequence Deletion
  • Spleen / cytology
  • T-Lymphocytes / immunology
  • Thymus Gland / cytology
  • Transcription Factors / deficiency
  • Transcription Factors / genetics
  • Transcription Factors / physiology*


  • CD8 Antigens
  • DNA-Binding Proteins
  • Transcription Factors
  • Zfpn1a1 protein, mouse
  • Ikaros Transcription Factor