Deficiency of transcription factor RelB perturbs myeloid and DC development by hematopoietic-extrinsic mechanisms
Copyright policy )Deficiency of transcription factor RelB perturbs myeloid and DC development by hematopoietic-extrinsic mechanisms
SignificanceThe transcription factor RelB has been thought to be required for dendritic cell (DC) development, although analysis of radiation bone marrow chimeras has raised some questions regarding this issue that have never been resolved. We have reevaluated the role of RelB in DC and myeloid development. We found that DC development was independent of a cell-intrinsic action of RelB in most tissues and that only the terminal maturation of Notch2-dependent splenic cDC2 cells was partially reduced in the absence of cell-intrinsic RelB expression. Moreover, the profound myeloid expansion seen inRelb−/−mice was due to an unrecognized action of RelB in nonhematopoietic cells, indicating that RelB is a critical component of the niche regulating the normal myeloid compartment.
- University of Mary United States
- Washington University in St. Louis United States
- Howard Hughes Medical Institute United States
CD4-Positive T-Lymphocytes, Lymphotoxin-beta, Hematopoietic System, Transcription Factor RelB, Dendritic Cells, CD8-Positive T-Lymphocytes, Protein Serine-Threonine Kinases, Mice, Mutant Strains, Mice, Inbred C57BL, Lymphotoxin beta Receptor, NF-kappaB-Inducing Kinase, Animals, Myeloid Cells, Spleen
CD4-Positive T-Lymphocytes, Lymphotoxin-beta, Hematopoietic System, Transcription Factor RelB, Dendritic Cells, CD8-Positive T-Lymphocytes, Protein Serine-Threonine Kinases, Mice, Mutant Strains, Mice, Inbred C57BL, Lymphotoxin beta Receptor, NF-kappaB-Inducing Kinase, Animals, Myeloid Cells, Spleen
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