Journal article
Notch2 Receptor Signaling Controls Functional Differentiation of Dendritic Cells in the Spleen and Intestine
Immunity, Vol.35(5), pp.780-791
Nov/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 Esamh 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.
Details
- Title
- Notch2 Receptor Signaling Controls Functional Differentiation of Dendritic Cells in the Spleen and Intestine
- Creators
- Kanako L. Lewis (null)Michele L. Caton (null)Milena Bogunovic (null)Melanie Greter (null)Lucja T. Grajkowska (null)Dennis Ng (null)Apostolos Klinakis (null)Israel F. Charo (null)Steffen Jung (null) - 972WIS_INST___120Jennifer L. Gommerman (null)Ivaylo I. Ivanov (null)Kang Liu (null)Miriam Merad (null)Boris Reizis (null)
- Resource Type
- Journal article
- Publication Details
- Immunity, Vol.35(5), pp.780-791; Nov/2011
- Number of pages
- 12
- Language
- English
- DOI
- https://doi.org/10.1016/j.immuni.2011.08.013
- Grant note
- American Asthma Foundation; NIH [AI072571, DK085329, AI007161, HD055165]; CIHR/IRSC [67157]We thank U. Klein, A. Efstratiadis, F. Radtke, T. Gridley, and W. Pear for mouse strains; A. Capobianco, D. Lin, and A. Ferrante for animal donations; M. Lahoud for antibodies; and J. Ericson for Immgen data. Supported by the American Asthma Foundation (B.R.), NIH grants AI072571 (B.R.) and DK085329 (I.I.I.), NIH training grants AI007161 (K.L.L.) and HD055165 (M.L.C.), and CIHR/IRSC award MOP #67157 (J.L.G.)._ALMAME_DELIMITER_
- Record Identifier
- 993264979203596
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