The Journal of Experimental Medicine
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Published 15 October 2001. doi:10.1084/jem.194.8.1171
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© The Rockefeller University Press, 0022-1007/2001/10/1171/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 8, October 15, 2001 1171-1178


Brief Definitive Report

CD11c+B220+Gr-1+ Cells in Mouse Lymph Nodes and Spleen Display Characteristics of Plasmacytoid Dendritic Cells

Hideki Nakanoa, Manabu Yanagitaa, and Michael Dee Gunna,b
a Department of Medicine and Division of Cardiology, Duke University Medical Center, Durham, NC 27710
b Department of Immunology, Duke University Medical Center, Durham, NC 27710

Correspondence to: Michael Dee Gunn, Box 3547, Duke University Medical Center, Durham, NC 27710. Tel:919-681-0840 Fax:919-684-8591 E-mail:michael.gunn{at}duke.edu.

Human plasmacytoid dendritic cells (pDCs) are major producers of IFN{alpha}, are activated by CpG motifs, and are believed to enter lymph nodes (LNs) via L-selectin dependent extravasation across high endothelial venules. To identify a similar murine DC type, CD11c+ cells in the LNs of L-selectin–deficient and control BALB/c mice were compared, revealing a population of CD11c+CD11b- cells that is reduced 85% in the LNs of L-selectin–deficient mice. These cells are Gr-1+B220+CD19-, either CD4+ or CD8+, and localize within T cell zones of LNs. Freshly isolated CD11c+Gr-1+ cells express major histocompatibility complex class II at low levels, display a plasmacytoid morphology, and survive poorly in culture. Their survival is increased and they develop a DC-like morphology in interleukin 3 and CpG. Like human pDCs, CD11c+Gr-1+ cells stimulate T cell proliferation after activation with CpG and produce IFN{alpha} after stimulation with influenza virus. These cells also display a strain-specific variation in frequency, being fivefold increased in the LNs of BALB/c relative to C57BL/6 mice. These CD11c+CD11b-B220+Gr-1+ cells appear to be the murine equivalent of human pDCs.

Key Words: dendritic cells, lymph nodes, B220 antigens, L-selectin, interferon type 1


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