The Journal of Experimental Medicine
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Published online June 25, 2007
doi:10.1084/jem.20062648
The Journal of Experimental Medicine, Vol. 204, No. 7, 1653-1664
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Caton et al.
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ARTICLE

 Notch–RBP-J signaling controls the homeostasis of CD8– dendritic cells in the spleen

Michele L. Caton, Matthew R. Smith-Raska, and Boris Reizis

Department of Microbiology, Columbia University Medical Center, New York, NY, 10032

CORRESPONDENCE Boris Reizis: bvr2101{at}columbia.edu

Signaling through Notch receptors and their transcriptional effector RBP-J is essential for lymphocyte development and function, whereas its role in other immune cell types is unclear. We tested the function of the canonical Notch–RBP-J pathway in dendritic cell (DC) development and maintenance in vivo. Genetic inactivation of RBP-J in the bone marrow did not preclude DC lineage commitment but caused the reduction of splenic DC fraction. The inactivation of RBP-J in DCs using a novel DC-specific deleter strain caused selective loss of the splenic CD8– DC subset and reduced the frequency of cytokine-secreting CD8– DCs after challenge with Toll-like receptor ligands. In contrast, other splenic DC subsets and DCs in the lymph nodes and tissues were unaffected. The RBP-J–deficient splenic CD8– DCs were depleted at the postprogenitor stage, exhibited increased apoptosis, and lost the expression of the Notch target gene Deltex1. In the spleen, CD8– DCs were found adjacent to cells expressing the Notch ligand Delta-like 1 in the marginal zone (MZ). Thus, canonical Notch–RBP-J signaling controls the maintenance of CD8– DCs in the splenic MZ, revealing an unexpected role of the Notch pathway in the innate immune system.

Abbreviations used: BAC, bacterial artificial chromosome; CKO, conditional knockout; Dll1, Delta-like 1; EYFP, enhanced yellow fluorescent protein; IRF, interferon regulatory factor; MZ, marginal zone; PDC, plasmacytoid dendritic cell; qPCR, quantitative real-time PCR; TLR, Toll-like receptor.


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