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RelB is essential for the development of myeloid-related CD8 alpha(-) dendritic cells but not of lymphoid-related CD8 alpha(+) dendritic cells


Wu, L; D'Amico, A; Winkel, KD; Suter, M; Lo, D; Shortman, K
1998-12
IMMUNITY
Journal Article
9
6
839-847
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 CD8 alpha(-) DEC-205(-) DC but only weakly in CD8 alpha(+) DEC-205(+) DC. In addition, CD8 alpha(+) DEC-205(+) DC are present and functional in RelB null mice, the DC deficiency being mainly in the CD8 alpha(-) 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 CD8 alpha(-) DEC-205(-) DC is a direct, stem cell intrinsic effect of the RelB mutation. Thus, RelB selectively regulates a myeloid-related DC lineage.
CELL PRESS
COLONY-STIMULATING FACTOR; LIGAND-TREATED MICE; T-CELLS; SURFACE-MARKERS; MOUSE THYMUS; IN-VIVO; EXPRESSION; MATURATION; PHENOTYPE; PATHWAYS
10.1016/S1074-7613(00)80649-4
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