| Autor: |
Spits, Hergen, Couwenberg, Franka, Bakker, Arjen Q., Weijer, Kees, Uittenbogaart, Christel H. |
| Zdroj: |
The Journal of Experimental Medicine; December 2000, Vol. 192 Issue: 12 p1775-1784, 10p |
| Abstrakt: |
We found previously that Id3, which inhibits transcriptional activities of many basic helix-loop-helix transcription factors, blocked T and B cell development but stimulated natural killer (NK) cell development. Here we report that ectopic expression of Id3 and another Id protein, Id2, strongly inhibited the development of primitive CD34+CD38− progenitor cells into CD123high dendritic cell (DC)2 precursors. In contrast, development of CD34+CD38− cells into CD4+CD14+ DC1 precursors and mature DC1 was not affected by ectopic Id2 or Id3 expression. These observations support the notion of a common origin of DC2 precursors, T and B cells. As Id proteins did not block development of NK cells, a model presents itself in which these proteins drive common lymphoid precursors to develop into NK cells by inhibiting their options to develop into T cells, B cells, and pre-DC2. |
| Databáze: |
Supplemental Index |
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