ArticleJournal of immunology (Baltimore, Md. : 1950)2011
MyD88-dependent SHIP1 regulates proinflammatory signaling pathways in dendritic cells after monophosphoryl lipid A stimulation of TLR4.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Monosaccharide-Based Synthetic TLR4 Agonist Enhances Vaccine Efficacy againstACS infectious diseases · 2025Article
- SHIP-1 Differentially Regulates IgE-Induced IL-10 and Antiviral Responses in Human Monocytes.European journal of immunology · 2025Article
- Article
- Cell-intrinsic and -extrinsic roles of miRNAs in regulating T cell immunity.Immunological reviews · 2021Review
- Mechanisms of TLR4-Mediated Autophagy and Nitroxidative Stress.Frontiers in cellular and infection microbiology · 2021Review
- MicroRNA-155: Regulation of Immune Cells in Sepsis.Mediators of inflammation · 2021Review
- Stroma: the forgotten cells of innate immune memory.Clinical and experimental immunology · 2018Review
- Specific features of human monocytes activation by monophosphoryl lipid A.Scientific reports · 2018Article
- An NF-κB-microRNA regulatory network tunes macrophage inflammatory responses.Nature communications · 2017Article
- MicroRNA-155 Mediates Augmented CD40 Expression in Bone Marrow Derived Plasmacytoid Dendritic Cells in Symptomatic Lupus-Prone NZB/W F1 Mice.International journal of molecular sciences · 2016Article
- Monophosphoryl lipid A inhibits the cytokine response of endothelial cells challenged with LPS.Innate immunity · 2015Article
- The cholesterol transporter ABCG1 links cholesterol homeostasis and tumour immunity.Nature communications · 2015Article
- Genome-wide immunity studies in the rabbit: transcriptome variations in peripheral blood mononuclear cells after in vitro stimulation by LPS or PMA-Ionomycin.BMC genomics · 2015Article
- Myeloid expression of adenosine A2A receptor suppresses T and NK cell responses in the solid tumor microenvironment.Cancer research · 2014Article
- TLR4-mediated expression of Mac-1 in monocytes plays a pivotal role in monocyte adhesion to vascular endothelium.PloS one · 2014Article
- Extracellular adenosine regulates naive T cell development and peripheral maintenance.The Journal of experimental medicine · 2013Article
- Characterization of AQX-1125, a small-molecule SHIP1 activator: Part 2. Efficacy studies in allergic and pulmonary inflammation models in vivo.British journal of pharmacology · 2013Article
- Article
- In vivo and in vitro characterization of the immune stimulating activity of the Neisserial porin PorB.PloS one · 2013Article
- Immunopharmacology of lipid A mimetics.Advances in pharmacology (San Diego, Calif.) · 2013Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
We previously showed that monophosphoryl lipid A (MLA) activates TLR4 in dendritic cells (DCs) in a Toll/IL-1R domain-containing adaptor inducing IFN-β (TRIF)-biased manner: MLA produced from Salmonella minnesota Re595 induced signaling events and expression of gene products that were primarily TRIF dependent, whereas MyD88-dependent signaling was impaired. Moreover, when tested in TRIF-intact/MyD88-deficient DCs, synthetic MLA of the Escherichia coli chemotype (sMLA) showed the same activity as its diphosphoryl, inflammatory counterpart (synthetic diphosphoryl lipid A), indicating that TRIF-mediated signaling is fully induced by sMLA. Unexpectedly, we found that the transcript level of one proinflammatory cytokine was increased in sMLA-treated cells by MyD88 deficiency to the higher level induced by synthetic diphosphoryl lipid A, which suggested MyD88 may paradoxically help restrain proinflammatory signaling by TRIF-biased sMLA. In this article, we demonstrate that sMLA induces MyD88 recruitment to TLR4 and activates the anti-inflammatory lipid phosphatase SHIP1 in an MyD88-dependent manner. At the same time, MyD88-dependent signaling activity at the level of IL-1R-associated kinase 1 is markedly reduced. Increased SHIP1 activity is associated with reductions in sMLA-induced IκB kinase α/β and IFN regulatory factor 3 activation and with restrained expression of their downstream targets, endothelin-1 and IFN-β, respectively. Results of this study identify a pattern that is desirable in the context of vaccine adjuvant design: TRIF-biased sMLA can stimulate partial MyD88 activity, with MyD88-dependent SHIP1 helping to reduce proinflammatory signaling in DCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.