Macrophages and myeloid dendritic cells, but not plasmacytoid dendritic cells, produce IL-10 in response to MyD88- and TRIF-dependent TLR signals, and TLR-independent signals

André Boonstra, Ricardo Rajsbaum, Mary Holman, Rute Marques, Carine Asselin-Paturel, João Pedro Pereira, Elizabeth E.M. Bates, Shizuo Akira, Paulo Vieira, Yong Jun Liu, Giorgio Trinchieri, Anne O'Garra

Research output: Contribution to journalArticlepeer-review

219 Scopus citations

Abstract

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 CD8α- and CD8α+ DC. Although plasmacytoid DC did not produce EL-10 upon stimulation, addition of this cytokine exogenously suppressed their production of IL-12, TNF, and IFN-α, showing trans but not autocrine regulation of these cytokines by IL-10 in plasmacytoid DC.

Original languageEnglish (US)
Pages (from-to)7551-7558
Number of pages8
JournalJournal of Immunology
Volume177
Issue number11
DOIs
StatePublished - Dec 1 2006
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Macrophages and myeloid dendritic cells, but not plasmacytoid dendritic cells, produce IL-10 in response to MyD88- and TRIF-dependent TLR signals, and TLR-independent signals'. Together they form a unique fingerprint.

Cite this