Article abstract
Nature Immunology 10, 394 - 402 (2009)
Published online: 1 March 2009 | doi:10.1038/ni.1707
Blood-derived inflammatory dendritic cells in lymph nodes stimulate acute T helper type 1 immune responses
Hideki Nakano1,2,3,6, Kaifeng Lisa Lin2,6, Manabu Yanagita1,5, Chantal Charbonneau1, Donald N Cook3, Terutaka Kakiuchi4 & Michael D Gunn1,2
Abstract
T helper type 1 (TH1)-polarized immune responses, which confer protection against intracellular pathogens, are thought to be initiated by dendritic cells (DCs) that enter lymph nodes from peripheral tissues. Here we found after viral infection or immunization, inflammatory monocytes were recruited into lymph nodes directly from the blood to become CD11c+CD11bhiGr-1+ inflammatory DCs, which produced abundant interleukin 12p70 and potently stimulated TH1 responses. This monocyte extravasation required the chemokine receptor CCR2 but not the chemokine CCL2 or receptor CCR7. Thus, the accumulation of inflammatory DCs and TH1 responses were much lower in Ccr2-/- mice, were preserved in Ccl2-/- mice and were relatively higher in CCL19–CCL21-Ser–deficient plt mutant mice, in which all other lymph node DC types were fewer in number. We conclude that blood-derived inflammatory DCs are important in the development of TH1 immune responses.
- Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.
- Department of Immunology, Duke University Medical Center, Durham, North Carolina, USA.
- Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.
- Department of Immunology, Toho University School of Medicine, Tokyo, Japan.
- Present address: Department of Periodontology, Division of Oral Biology and Disease Control, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka, Japan.
- These authors contributed equally to this work.
Correspondence to: Michael D Gunn1,2 e-mail: michael.gunn@duke.edu
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