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The opposing roles of the transcription factor E2A and its antagonist Id3 that orchestrate and enforce the naive fate of T cells.

It is established that the transcription factor E2A and its antagonist Id3 modulate the checkpoints consisting of the precursor to the T cell antigen receptor (pre-TCR) and the TCR. Here we demonstrate that Id3 expression was higher beyond the pre-TCR checkpoint, remained high in naive T cells and showed a bimodal pattern in the effector-memory population. We show how E2A promoted T lineage specification and how pre-TCR-mediated signaling affected E2A genome-wide occupancy. Thymi in Id3-deficient mice had aberrant development of effector-memory cells, higher expression of the chemokine receptor CXCR5 and the transcriptional repressor Bcl-6 and, unexpectedly, T cell-B cell conjugates and B cell follicles. Collectively, our data show how E2A acted globally to orchestrate development into the T lineage and that Id3 antagonized E2A activity beyond the pre-TCR checkpoint to enforce the naive fate of T cells.

Pubmed ID: 21857655

Authors

  • Miyazaki M
  • Rivera RR
  • Miyazaki K
  • Lin YC
  • Agata Y
  • Murre C

Journal

Nature immunology

Publication Data

October 21, 2011

Associated Grants

  • Agency: NCI NIH HHS, Id: R01 CA078384
  • Agency: NCI NIH HHS, Id: R01 CA078384-10
  • Agency: NCI NIH HHS, Id: R37 CA054198
  • Agency: NCI NIH HHS, Id: R37 CA054198-18

Mesh Terms

  • Animals
  • Antigens, CD45
  • Basic Helix-Loop-Helix Transcription Factors
  • Immunologic Memory
  • Immunophenotyping
  • Inhibitor of Differentiation Proteins
  • Mice
  • Mice, Inbred C57BL
  • Receptors, Antigen, T-Cell
  • Receptors, CXCR5
  • Spleen
  • T-Lymphocytes
  • Thymus Gland