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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.

Nature immunology | Oct 21, 2011

http://www.ncbi.nlm.nih.gov/pubmed/21857655

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 RIS Download

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

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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

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