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Original Article |
Correspondence to: Hergen Spits, Div. of Immunology, Netherlands Cancer Institute, Plesmanlaan 121, 10066 CX Amsterdam, Netherlands. Tel:31-20-512-2063 Fax:31-20-512-2057 E-mail:hergen{at}nki.nl.
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.
Key Words: dendritic cells, dendritic cell precursors, basic helix-loop-helix transcription factors, idiotype proteins, lymphoid development
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