期刊
NATURE IMMUNOLOGY
卷 17, 期 7, 页码 834-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3461
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资金
- US National Institutes of Health [1F31AG043222-01A1, AI108651, AI067545, AI109976]
- Fonds de la recherche Quebec-Sante
- Damon Runyon Cancer Research Foundation (Fraternal Order of Eagles Fellowship) [DRG-2069-11]
- Leukemia and Lymphoma Society
The differentiation of helper T cells into effector subsets is critical to host protection. Transcription factors of the E-protein and Id families are important arbiters of T cell development, but their role in the differentiation of the T(H)1 and T-FH subsets of helper T cells is not well understood. Here, T(H)1 cells showed more robust Id2 expression than that of T-FH cells, and depletion of Id2 via RNA-mediated interference increased the frequency of T-FH cells. Furthermore, T(H)1 differentiation was blocked by Id2 deficiency, which led to E-protein-dependent accumulation of effector cells with mixed characteristics during viral infection and severely impaired the generation of T(H)1 cells following infection with Toxoplasma gondii. The T-FH cell-defining transcriptional repressor Bcl6 bound the Id2 locus, which provides a mechanism for the bimodal Id2 expression and reciprocal development of T(H)1 cells and T-FH cells.
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