Abstract
The transcription factor RelB had been shown to be important for dendritic cell (DC) development, but the type of DC involved was not clear. Here, we report that RelB mRNA is expressed strongly in CD8alpha- DEC-205- DC but only weakly in CD8alpha+ DEC-205+ DC. In addition, CD8alpha+ DEC-205+ DC are present and functional in RelB null mice, the DC deficiency being mainly in the CD8alpha- DEC-205- population. By constructing bone-marrow chimeric mice, we demonstrate that the partial deficiency in RelB null thymic DC is a secondary effect of disrupted thymic architecture. However, the deficiency in splenic CD8alpha- DEC-205- DC is a direct, stem cell intrinsic effect of the RelB mutation. Thus, RelB selectively regulates a myeloid-related DC lineage.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigen Presentation
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Antigens, CD*
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CD8 Antigens*
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Cell Differentiation
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Cells, Cultured
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Dendritic Cells / cytology*
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Dendritic Cells / metabolism*
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Epidermis
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Langerhans Cells / cytology
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Lectins, C-Type*
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Lymphocytes
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Membrane Glycoproteins*
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Mice
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Mice, Inbred C57BL
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Mice, Mutant Strains
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Minor Histocompatibility Antigens
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism*
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RNA, Messenger
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Receptors, Cell Surface*
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Spleen / cytology
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Thymus Gland / cytology
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Transcription Factor RelB
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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Antigens, CD
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CD8 Antigens
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DEC-205 receptor
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Lectins, C-Type
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Membrane Glycoproteins
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Minor Histocompatibility Antigens
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Proto-Oncogene Proteins
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RNA, Messenger
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Receptors, Cell Surface
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Relb protein, mouse
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Transcription Factors
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Transcription Factor RelB