ArticleImmunity, inflammation and disease2017
The Mincle ligand trehalose dibehenate differentially modulates M1-like and M2-like macrophage phenotype and function via Syk signaling.
Article in Immunity, inflammation and disease, 2017. 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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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- The role of gut mycobiome in responses to cancer immunotherapy.Gut microbes · 2025Review
- Approaches to stereoselective 1,1'-glycosylation.Beilstein journal of organic chemistry · 2025Review
- Article
- Review
- Probing Isosteric Replacement for Immunoadjuvant Design: Bis-Aryl Triazole Trehalolipids are Mincle Agonists.ACS medicinal chemistry letters · 2024Article
- Aryl-functionalised α,α'-Trehalose 6,6'-Glycolipid Induces Mincle-independent Pyroptotic Cell Death.Inflammation · 2023Article
- Thermophobic Trehalose Glycopolymers as Smart C-Type Lectin Receptor Vaccine Adjuvants.Advanced healthcare materials · 2023Article
- Versatile approach towards fully desymmetrized trehalose with a novel set of orthogonal protecting groups.Frontiers in chemistry · 2023Article
- TH17 cells promote CNS inflammation by sensing danger signals via Mincle.Nature communications · 2022Article
- SYK Is Associated With Malignant Phenotype and Immune Checkpoints in Diffuse Glioma.Frontiers in genetics · 2022Article
- Water-soluble trehalose glycolipids show superior Mincle binding and signaling but impaired phagocytosis and IL-1β production.Frontiers in molecular biosciences · 2022Article
- USMB-shMincle: a virus-free gene therapy for blocking M1/M2 polarization of tumor-associated macrophages.Molecular therapy oncolytics · 2021Article
- Emerging glyco-based strategies to steer immune responses.The FEBS journal · 2021Review
- Lyophilization Preserves the Intrinsic Cardioprotective Activity of Bioinspired Cell-Derived Nanovesicles.Pharmaceutics · 2021Article
- Orientia tsutsugamushi selectively stimulates the C-type lectin receptor Mincle and type 1-skewed proinflammatory immune responses.PLoS pathogens · 2021Article
- Type I IFN, Ly6CMolecular cancer therapeutics · 2020Article
- Mycobacterial Trehalose 6,6'-Dimycolate-Induced M1-Type Inflammation.The American journal of pathology · 2020Article
- The Role of Macrophage-Inducible C-Type Lectin in Different Stages of Chronic Liver Disease.Frontiers in immunology · 2020Article
- MSU Crystals Enhance TDB-Mediated Inflammatory Macrophage IL-1β Secretion.Inflammation · 2019Article
- The effects of trehalose glycolipid presentation on cytokine production by GM-CSF macrophages.Glycoconjugate journal · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMacrophages play a significant role in the progression of diseases, such as cancer, making them a target for immune-modulating agents. Trehalose dibehenate (TDB) is known to activate M1-like macrophages via Mincle, however, the effect of TDB on M2-like macrophages, which are found in the tumor microenvironment, has not been studied.
methodsqRT-PCR, flow cytometry, cytokine ELISA, and Western Blotting were used to study the effect of TDB on GM-CSF and M-CSF/IL-4 derived bone marrow macrophages (BMMs) from C57BL/6 and Mincle
resultsTDB treatment up-regulated M1 markers over M2 markers by GM-CSF BMMs, whereas M-CSF/IL-4 BMMs down-regulated marker gene expression overall. TDB treatment resulted in Mincle-independent down-regulation of CD11b, CD115, and CD206 expression by GM-CSF macrophages and CD115 in M-CSF/IL-4 macrophages. GM-CSF BMMs produced of significant levels of proinflammatory cytokines (IL-1β, IL-6, TNF-α), which was Mincle-dependent and further enhanced by LPS priming. M-CSF BMMs produced little or no cytokines in response to TDB regardless of LPS priming. Western blot analysis confirmed that the absence of cytokine production was associated with a lack of activation of the Syk kinase pathway.
conclusionThis study illustrates that TDB has the potential to differentially regulate M1- and M2-like macrophages in the tumor environment.
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