Notch2 receptor signaling controls functional differentiation of dendritic cells in the spleen and intestine

ABSTRACT: Dendritic cells (DCs) in tissues and lymphoid organs comprise distinct functional subsets that differentiate in situ from circulating progenitors. Tissue-specific signals that regulate DC subset differentiation are poorly understood. We report that DC-specific deletion of the Notch2 receptor caused a reduction of DC populations in the spleen. Within the splenic CD11b+ DCs, Notch signaling blockade ablated a distinct population marked by high expression of adhesion molecule Esam. The Notch-dependent Esamhi DC subset also required lymphotoxin beta receptor signaling, proliferated in situ and facilitated efficient CD4+ T cell priming. The Notch-independent Esamlo DCs expressed monocyte-related genes and showed superior cytokine responses. In addition, Notch2 deletion led to the loss of CD11b+

ORGANISM(S): Mus musculus

SUBMITTER: Boris Reizis 

PROVIDER: E-GEOD-31551 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress