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* Division of Immunoregulation, National Institute for Medical Research, London, United Kingdom;
Laboratory for Immunological Research, Schering-Plough, Dardilly, France;
Instituto de Ciencias da Vida e Saude, Escola de Ciencias da Saude, Universidade Minho, Braga, Portugal;
Unité du Développement des Lymphocytes, Institute Pasteur, Paris, France;
¶ Department of Immunology, University of Texas, M. D. Anderson Cancer Center, Houston, TX 77030;
|| Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; and
# Exploratory Research for Advanced Technology (Japan), Japan Science and Technology Agency, Osaka, Japan
We have previously reported that mouse plasmacytoid dendritic cells (DC) produce high levels of IL-12p70, whereas bone marrow-derived myeloid DC and splenic DC produce substantially lower levels of this cytokine when activated with the TLR-9 ligand CpG. We now show that in response to CpG stimulation, high levels of IL-10 are secreted by macrophages, intermediate levels by myeloid DC, but no detectable IL-10 is secreted by plasmacytoid DC. MyD88-dependent TLR signals (TLR4, 7, 9 ligation), Toll/IL-1 receptor domain-containing adaptor-dependent TLR signals (TLR3, 4 ligation) as well as non-TLR signals (CD40 ligation) induced macrophages and myeloid DC to produce IL-10 in addition to proinflammatory cytokines. IL-12p70 expression in response to CpG was suppressed by endogenous IL-10 in macrophages, in myeloid DC, and to an even greater extent in splenic CD8
– and CD8+ DC. Although plasmacytoid DC did not produce IL-10 upon stimulation, addition of this cytokine exogenously suppressed their production of IL-12, TNF, and IFN-, showing trans but not autocrine regulation of these cytokines by IL-10 in plasmacytoid DC.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by the Medical Research Council, United Kingdom, and the European Community (Grant Framework 6 Programme: DC-VACC).
2 Address correspondence and reprint requests to Dr. Anne O’Garra, Division of Immunoregulation, National Institute for Medical Research, The Ridgeway, London, NW7 1AA, U.K. E-mail address: aogarra{at}nimr.mrc.ac.uk
3 Abbreviations used in this paper: DC, dendritic cell; pDC, plasmacytoid dendritic cell; BM, bone marrow; KO, knockout; TRIF, Toll/IL-1 receptor domain-containing adaptor.
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