期刊
NATURE IMMUNOLOGY
卷 12, 期 10, 页码 992-U103出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2086
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资金
- American Recovery and Investment Act [27775A]
- US National Institutes of Health
- Grants-in-Aid for Scientific Research [23390068, 22021021] Funding Source: KAKEN
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.
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