ArticleFrontiers in immunology2018
Dendritic Cells Actively Limit Interleukin-10 Production Under Inflammatory Conditions
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
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- Identification of Highly Repetitive Enhancers with Long-range Regulation Potential in Barley via STARR-seq.Genomics, proteomics & bioinformatics · 2024Article
- Systematic identification of genomic elements that regulate FCGR2A expression and harbor variants linked with autoimmune disease.Human molecular genetics · 2022Article
- Immune Regulatory Processes of the Tumor Microenvironment under Malignant Conditions.International journal of molecular sciences · 2021Review
- Innate immune signatures to a partially-efficacious HIV vaccine predict correlates of HIV-1 infection risk.PLoS pathogens · 2021Article
- PD-1/PD-L1 Checkpoint Inhibitors in Tumor Immunotherapy.Frontiers in pharmacology · 2021Review
- Cell-free miR-17-5p as a diagnostic biomarker for gastric cancer inhibits dendritic cell maturation.OncoTargets and therapy · 2019Article
- A Threshold Model for T-Cell Activation in the Era of Checkpoint Blockade Immunotherapy.Frontiers in immunology · 2019Review
- Rare coding variant analysis in a large cohort of Ashkenazi Jewish families with inflammatory bowel disease.Human genetics · 2018Article
- Enhancement of Antitumor Vaccination by Targeting Dendritic Cell-Related IL-10.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cell (DC)-based immunotherapy makes use of the DC's ability to direct the adaptive immune response toward activation or inhibition. DCs perform this immune orchestration in part by secretion of selected cytokines. The most potent anti-inflammatory cytokine interleukin-10 (IL-10) is under tight regulation, as it needs to be predominantly expressed during the resolution phase of the immune response. Currently it is not clear whether there is active suppression of IL-10 by DCs at the initial pro-inflammatory stage of the immune response. Previously, knockdown of the DC-specific transcription factor DC-SCRIPT has been demonstrated to mediate an extensive increase in IL-10 production upon encounter with pro-inflammatory immune stimuli. Here, we explored how DC-SCRIPT contributes to IL-10 suppression under pro-inflammatory conditions by applying chromatin immunoprecipitation sequencing analysis of DC-SCRIPT and the epigenetic marks H3K4me3 and H3K27ac in human DCs. The data showed binding of DC-SCRIPT to a GA-rich motif at H3K27ac-marked genomic enhancers that associated with genes encoding MAPK dual-specificity phosphatases (DUSPs). Functional studies revealed that upon knockdown of DC-SCRIPT, human DCs express much less DUSP4 and exhibit increased phosphorylation of the three major MAPKs (ERK, JNK, and p38). Enhanced ERK signaling in DC-SCRIPT-knockdown-DCs led to higher production of IL-10, which was reverted by rescuing DUSP4 expression. Finally, DC-SCRIPT-knockdown-DCs induced less IFN-γ and increased IL-10 production in naïve T cells, indicative for a more anti-inflammatory phenotype. In conclusion, we have delineated a new mechanism by which DC-SCRIPT allows DCs to limit IL-10 production under inflammatory conditions and potentiate pro-inflammatory Th1 responses. These insights may be exploited to improve DC-based immunotherapies.
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