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Notch2 Receptor Signaling Controls Functional Differentiation of Dendritic Cells in the Spleen and Intestine
- Source :
- Immunity. 35:780-791
- Publication Year :
- 2011
- Publisher :
- Elsevier BV, 2011.
-
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(+) DC subset, Notch signaling blockade ablated a distinct population marked by high expression of the adhesion molecule Esam. The Notch-dependent Esam(hi) DC subset required lymphotoxin beta receptor signaling, proliferated in situ, and facilitated CD4(+) T cell priming. The Notch-independent Esam(lo) DCs expressed monocyte-related genes and showed superior cytokine responses. In addition, Notch2 deletion led to the loss of CD11b(+)CD103(+) DCs in the intestinal lamina propria and to a corresponding decrease of IL-17-producing CD4(+) T cells in the intestine. Thus, Notch2 is a common differentiation signal for T cell-priming CD11b(+) DC subsets in the spleen and intestine.
- Subjects :
- Male
T cell
Immunology
Population
Notch signaling pathway
Priming (immunology)
Mice, Transgenic
Spleen
Biology
Article
Mice
medicine
Animals
Immunology and Allergy
Receptor, Notch2
Intestinal Mucosa
education
Cells, Cultured
education.field_of_study
Gene Expression Profiling
Gene Expression Regulation, Developmental
Cell Differentiation
Dendritic Cells
Cell biology
Intestines
Mice, Inbred C57BL
Phenotype
Infectious Diseases
medicine.anatomical_structure
fms-Like Tyrosine Kinase 3
Immunoglobulin J Recombination Signal Sequence-Binding Protein
Female
Signal transduction
Lymphotoxin beta receptor
Conventional Dendritic Cell
Signal Transduction
Subjects
Details
- ISSN :
- 10747613
- Volume :
- 35
- Database :
- OpenAIRE
- Journal :
- Immunity
- Accession number :
- edsair.doi.dedup.....eb9c12daef54ede245d86ab4d2503671