期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 11, 页码 7551-7558出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.11.7551
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- Medical Research Council [MC_U117565642] Funding Source: Medline
- MRC [MC_U117565642] Funding Source: UKRI
- Medical Research Council [MC_U117565642] Funding Source: researchfish
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 alpha(-) and CD8 alpha(+) 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-alpha, showing trans but not autocrine regulation of these cytokines by IL-10 in plasmacytoid DC. The Journal of Immunology, 2006, 177: 7551-7558.
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