Affinage

CLEC4E

C-type lectin domain family 4 member E · UniProt Q9ULY5

Length
219 aa
Mass
25.1 kDa
Annotated
2026-04-28
100 papers in source corpus 47 papers cited in narrative 47 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CLEC4E (Mincle) is a myeloid- and TH17-cell-expressed C-type lectin receptor that functions as a pattern-recognition receptor for microbial glycolipids and endogenous damage-associated molecular patterns, coupling innate danger sensing to proinflammatory signaling and adaptive immune polarization. Mincle recognizes diverse ligands—including mycobacterial trehalose dimycolate (TDM), bacterial glucosyl-diacylglycerols, fungal α-mannose, and host-derived β-glucosylceramide, cholesterol, cholesterol sulfate, SAP130, and peroxiredoxin 1—through a Ca²⁺-dependent primary sugar-binding site and an adjacent hydrophobic groove in its C-type lectin domain that accommodates acyl chains (PMID:24101491, PMID:23960080, PMID:28373578, PMID:26296894, PMID:18776906, PMID:37164261). Upon ligand engagement, Mincle associates with the ITAM-bearing adaptor FcRγ and signals through Syk–CARD9–Bcl10–MALT1 to activate NF-κB, driving proinflammatory cytokine and nitric oxide production, autophagy, macrophage pyroptosis, and TH17 differentiation; surface expression is positively regulated by MyD88/TLR/NF-κB and C/EBPβ transcription and stabilized by heterodimerization with MCL via its stalk region (PMID:18776906, PMID:23630357, PMID:25156364, PMID:25888641, PMID:27005451, PMID:35504893). Mincle signaling is negatively regulated by a CD11b–Lyn–SIRPα–SHP1 complex that dephosphorylates Syk and by an inhibitory ITAM (ITAMi) configuration induced by pathogens such as Leishmania, and dysregulated Mincle activity contributes to atherosclerosis, ischemia-reperfusion injury, neuroinflammation, and tumor immune evasion (PMID:29400702, PMID:27742545, PMID:27587433, PMID:27049944, PMID:34466750).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2008 High

    Identifying Mincle's signaling adaptor and first endogenous ligand established it as an innate sensor of non-homeostatic cell death: Mincle couples to FcRγ to activate macrophages, and SAP130 released from dead cells triggers neutrophil infiltration via this axis.

    Evidence Co-immunoprecipitation, Mincle-deficient macrophages, antibody blockade in vivo

    PMID:18776906

    Open questions at the time
    • Structural basis of SAP130–Mincle interaction undefined
    • Mechanism by which SAP130 is exposed or released from dead cells not determined
  2. 2009 High

    Identification of TDM and α-mannose as microbial Mincle ligands revealed Mincle as a bona fide pattern-recognition receptor for mycobacteria and Malassezia, broadening its role from DAMP to PAMP sensing.

    Evidence Lipid fractionation, glycoconjugate microarray, site-directed mutagenesis of mannose-binding motif, Mincle-deficient mice challenged with TDM or Malassezia

    PMID:19171887 PMID:20008526

    Open questions at the time
    • Relative contribution of different mycobacterial glycolipids in whole-organism context not resolved
    • Downstream signaling pathway not yet mapped
  3. 2010 High

    Demonstrating FcRγ dependence for TDM/TDB responses and TH17 adjuvanticity placed Mincle in the ITAM-coupled CLR family and linked it to adaptive immune polarization.

    Evidence FcRγ and Mincle genetic KO mice, recombinant Mincle-Fc binding, tuberculosis subunit vaccine model

    PMID:20164423

    Open questions at the time
    • Whether Mincle–FcRγ coupling is direct or requires additional accessory proteins not resolved
  4. 2012 High

    Mincle expression on neutrophils and its role in TDM-induced cell adhesion via Src/Syk/MEK-dependent F-actin remodeling extended the receptor's functional relevance beyond macrophages.

    Evidence Mincle-KO mice, neutrophil depletion, kinase inhibitors, F-actin polymerization assays

    PMID:22496642

    Open questions at the time
    • Direct Mincle ligand on neutrophil surface vs. soluble TDM encounter not distinguished
  5. 2013 High

    Crystal structures of the Mincle CRD revealed dual binding determinants—a Ca²⁺-dependent sugar-binding site and an adjacent hydrophobic groove for acyl chains—explaining how Mincle recognizes glycolipids with both sugar headgroups and lipid tails, and the Syk–CARD9–Bcl10–MALT1 signaling cascade was mapped downstream.

    Evidence X-ray crystallography (human and bovine CRD), site-directed mutagenesis, synthetic analog binding, co-immunoprecipitation of MCL–Mincle–FcRγ, CARD9/caspase-1/ASC epistasis

    PMID:23630357 PMID:23921530 PMID:23960080 PMID:24101491

    Open questions at the time
    • Full-length receptor structure including transmembrane and stalk domains not determined
    • Structural basis of MCL heterodimerization not resolved at atomic level
  6. 2014 High

    Mincle was shown to engage pathogen-specific evasion mechanisms: Fonsecaea triggered Mdm2-dependent IRF1 degradation via Mincle–Syk–PKB, suppressing IL-12 and TH1 immunity; separately, NF-κB (not NFAT) was identified as the transcription factor binding the Mincle promoter downstream of Dectin-3/CARD9, defining a positive-feedback loop for Mincle expression.

    Evidence Genetic knockdown, signaling inhibitors, ChIP at Mincle promoter, Dectin-3-KO and CARD9-KO macrophages

    PMID:24721577 PMID:25202022

    Open questions at the time
    • Generalizability of IRF1 degradation mechanism to other Mincle ligands unknown
    • Whether NF-κB subunits other than p65 contribute not fully explored
  7. 2015 High

    MCL was established as a chaperone that stabilizes Mincle surface expression through its stalk region; hydrophobic residues in the MCL stalk are required, and MCL deficiency reduces Mincle protein without affecting mRNA.

    Evidence Co-IP, mutagenesis of MCL stalk, MCL-KO and transgenic mice, flow cytometry

    PMID:25888641

    Open questions at the time
    • Stoichiometry and oligomeric state of Mincle–MCL complex unknown
    • Whether MCL chaperone function extends to other CLRs not tested
  8. 2016 High

    A burst of discoveries in 2016 expanded Mincle biology in three directions: (1) identification of endogenous lipid ligands (cholesterol, cholesterol sulfate) and their role in atherosclerosis and contact dermatitis; (2) discovery of an ITAMi–SHP1 inhibitory mode exploited by Leishmania; and (3) demonstration that Mincle drives translational control of NO synthesis via p38/eIF5A hypusination and maintains M1 macrophage identity through TLR4/NF-κB-dependent transcription.

    Evidence Mincle-KO bone marrow chimeras in Ldlr-KO atherosclerosis model, cholesterol-binding reporter assays, conditional SHP1-KO in DCs, Mincle-KO macrophages with p38 inhibitors and eIF5A hypusination assays, NF-κB/p65 ChIP at Mincle promoter

    PMID:26296894 PMID:27089465 PMID:27587433 PMID:27742545 PMID:28017324 PMID:28292894

    Open questions at the time
    • Structural basis of species-specific cholesterol recognition (human but not mouse) unresolved
    • How ITAMi vs. activating ITAM switch is determined at molecular level not defined
    • Relative importance of transcriptional vs. translational control in different infection contexts unclear
  9. 2016 High

    Transcriptional regulation of Mincle was further refined: C/EBPβ was shown to be a central transcription factor for Mincle expression and TDM/TDB responsiveness, while MyD88 (not MCL) was identified as required for microbial-induced Mincle upregulation; MCL is constitutively expressed but retained intracellularly until Mincle induction allows heterodimer surface translocation.

    Evidence C/EBPβ-KO macrophages with retroviral Mincle rescue, MyD88-KO and MCL-KO macrophages, surface vs. intracellular flow cytometry

    PMID:25156364 PMID:27005451

    Open questions at the time
    • Whether C/EBPβ binds Mincle promoter directly or via intermediary factors not confirmed by ChIP
    • Intracellular retention mechanism of MCL not identified
  10. 2017 High

    β-Glucosylceramide was identified as a ubiquitous endogenous Mincle ligand released from damaged cells, establishing a lipid DAMP–Mincle axis validated by double-KO epistasis (GBA1/Mincle); species-specific ligand recognition was mapped to defined CRD residues for glycerol monomycolate, and acyl-chain branching was shown to govern glycolipid agonism.

    Evidence MS/NMR ligand identification, synthetic ligand validation, GBA1/Mincle double-KO mice, domain-swap chimeras, mutagenesis of positions 174–176 and 195–196

    PMID:24733387 PMID:28223515 PMID:28373578

    Open questions at the time
    • Physiological contexts in which β-GlcCer reaches threshold concentrations in vivo not comprehensively mapped
    • Full set of CRD residues governing species selectivity not enumerated
  11. 2018 High

    CD11b was identified as a negative regulator of Mincle signaling: mycobacterial activation triggers a Mincle–CD11b complex that recruits Lyn, SIRPα, and SHP1 to dephosphorylate Syk, providing a built-in brake on inflammation. MGDG from Group A Streptococcus was identified as another bacterial Mincle ligand critical for host defense.

    Evidence CD11b-KO macrophages and mice, co-IP of Mincle–CD11b–Lyn–SIRPα–SHP1, Mincle-KO mice infected with GAS

    PMID:29400702 PMID:30352847

    Open questions at the time
    • Whether CD11b inhibitory complex forms with all Mincle ligands or selectively with mycobacterial glycolipids not tested
    • Relative hierarchy of SHP1-mediated inhibition (ITAMi vs. CD11b axis) not established
  12. 2019 High

    Mincle–Syk signaling in dendritic cells was found to sense commensal microbiota in Peyer's patches, driving IL-6/IL-23-dependent intestinal TH17/ILC3 responses, RegIIIγ, and IgA—connecting Mincle to mucosal homeostasis beyond inflammation. Mincle also activated autophagy through MYD88 for intracellular Mtb restriction.

    Evidence Mincle-KO and DC-specific Syk conditional KO mice, intestinal immune profiling; Atg5-KO and Becn1-KD macrophages with autophagy flux assays

    PMID:30709742 PMID:31462144

    Open questions at the time
    • Specific commensal-derived Mincle ligands in the gut not identified
    • Whether Mincle-induced autophagy is selective (xenophagy) or bulk not distinguished
  13. 2020 High

    β-Glucosylceramide was confirmed as a Mincle ligand in renal ischemia-reperfusion injury, with free cholesterol acting as a co-agonist; Mincle was also linked to macrophage pyroptosis driving intestinal inflammation and to tumor-associated macrophage reprogramming via Syk/NF-κB in cancer.

    Evidence Mincle-KO mice in IRI and colitis models, MS lipid identification, Syk inhibitor in colitis, scRNA-seq and Mincle siRNA in syngeneic tumor models

    PMID:32333776 PMID:32532809 PMID:32797195

    Open questions at the time
    • Structural basis of cholesterol–β-GlcCer cooperativity at the CRD not resolved
    • Whether Mincle drives pyroptosis through canonical or non-canonical inflammasome pathways not fully distinguished
  14. 2021 High

    Peroxiredoxin 1 was identified as an additional protein DAMP ligand for Mincle in AKI, and SAP130-induced Mincle expression was shown to be post-transcriptionally repressed by miR-219c-3p binding the Mincle 3′-UTR, adding a miRNA-level regulatory layer.

    Evidence Prdx1-KO mice, co-IP of Prdx1–Mincle, recombinant rescue; miRNA 3′-UTR reporter assay, lentiviral miR-219c-3p overexpression in UUO mice

    PMID:34556635 PMID:37164261

    Open questions at the time
    • Binding site on Mincle CRD for protein DAMPs (Prdx1, SAP130) not structurally mapped
    • Broader miRNA regulatory landscape of Mincle unexplored
  15. 2022 High

    A T cell-intrinsic role for Mincle was established: β-GlcCer released during CNS inflammation activates Mincle on TH17 cells, triggering ASC–NLRP3 inflammasome assembly and Caspase-8-dependent IL-1β in an autocrine loop that sustains TH17 proliferation and EAE pathogenesis.

    Evidence T cell-specific Mincle conditional KO, NLRP3/ASC inflammasome assays, Caspase-8 inhibition, EAE model

    PMID:35504893

    Open questions at the time
    • Whether other T helper subsets express functional Mincle not systematically tested
    • Whether TH17 Mincle engagement occurs in human autoimmune disease not demonstrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis by which Mincle discriminates protein DAMPs (SAP130, Prdx1) from glycolipid ligands, the molecular determinants controlling the switch between activating ITAM and inhibitory ITAMi signaling modes, and whether therapeutic Mincle blockade can selectively dampen pathological inflammation without compromising antimicrobial defense.
  • No co-crystal structure of Mincle with any protein DAMP
  • Molecular switch between ITAM and ITAMi configuration structurally undefined
  • No clinical-stage Mincle-targeted therapeutic reported

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008289 lipid binding 5 GO:0060089 molecular transducer activity 4 GO:0140299 molecular sensor activity 4
Localization
GO:0005886 plasma membrane 4
Pathway
R-HSA-168256 Immune System 8 R-HSA-162582 Signal Transduction 6 R-HSA-5357801 Programmed Cell Death 2 R-HSA-9612973 Autophagy 1
Partners
CARD9CLEC4DFCER1GITGAMLYNPTPN6SIRPASYK
Complex memberships
CD11b–Lyn–SIRPα–SHP1 inhibitory complexMincle–FcRγ signaling complexMincle–MCL heterodimer

Evidence

Reading pass · 47 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 Mincle selectively associates with the Fc receptor common gamma-chain (FcRγ), an ITAM-bearing adaptor, to activate macrophages and produce inflammatory cytokines and chemokines. SAP130, a component of small nuclear ribonucleoprotein released from dead cells, was identified as a Mincle ligand, and Mincle-mediated sensing of non-homeostatic cell death drives neutrophil infiltration into damaged tissue. Co-immunoprecipitation, reporter cell assays, Mincle-specific antibody blockade in vivo, Mincle-deficient macrophages Nature immunology High 18776906
2009 Mincle is an essential receptor for the mycobacterial glycolipid trehalose-6,6'-dimycolate (TDM; cord factor). Delipidation of heat-killed mycobacteria abolished Mincle-expressing cell activation; lipid extract analysis identified TDM as the Mincle ligand. Mincle-deficient macrophages failed to produce inflammatory cytokines and nitric oxide in response to TDM, and Mincle-deficient mice did not form TDM-induced lung granulomas. Lipid fractionation, reporter cell assay, Mincle-deficient macrophages and mice, in vivo TDM challenge The Journal of experimental medicine High 20008526
2009 Mincle specifically recognizes Malassezia species among 50 fungal species tested. Mutation of the putative mannose-binding motif within the C-type lectin domain abolished Malassezia recognition. Glycoconjugate microarray showed Mincle selectively binds α-mannose but not mannan. Mincle-deficient mice had impaired cytokine/chemokine production and in vivo inflammatory responses to Malassezia. Reporter cell screening, site-directed mutagenesis, glycoconjugate microarray, Mincle-deficient mouse experiments Proceedings of the National Academy of Sciences of the United States of America High 19171887
2010 The FcRγ adaptor protein is essential for Mincle-mediated macrophage activation and Th17 adjuvanticity in response to TDM and its synthetic analog TDB. Recombinant Mincle-Fc fusion protein specifically binds these glycolipids. Genetic ablation of Mincle abolished TDM/TDB-induced macrophage activation and T cell immune responses to a tuberculosis subunit vaccine. Recombinant Mincle-Fc binding assay, genetic knockout of Mincle and FcRγ, in vivo vaccination experiments Journal of immunology (Baltimore, Md. : 1950) High 20164423
2013 Crystal structures of Mincle (and MCL) reveal Ca2+-dependent sugar binding and a unique shallow hydrophobic region adjacent to the sugar-binding site that accommodates the fatty acid moieties of glycolipids. Functional mutagenesis of residues in these regions confirmed the deduced binding mode for glycolipid recognition. X-ray crystallography of Mincle CRD, site-directed mutagenesis, functional reporter assays with glycolipid ligands Proceedings of the National Academy of Sciences of the United States of America High 24101491
2013 Crystallographic structural analysis and site-directed mutagenesis of bovine mincle CRD defined an extended binding site encompassing both the trehalose headgroup and a portion of attached acyl chains. One glucose residue of trehalose is liganded to Ca2+ in a manner common to C-type CRDs; the second glucose is accommodated in a novel secondary binding site providing 36-fold higher affinity for trehalose vs. glucose. An adjacent hydrophobic groove docks one acyl chain, allowing small molecule analogs to bind with 52-fold higher affinity than trehalose alone. X-ray crystallography, site-directed mutagenesis, binding studies with glycolipid mimics The Journal of biological chemistry High 23960080
2013 Upon receptor activation, Mincle signals via the Syk-CARD9-Bcl10-MALT1 pathway by recruiting the ITAM-bearing FcεRI-γ. MCL co-precipitates with FcεRI-γ via Mincle; Mincle and MCL form heteromers on the cell surface, and MCL/FcεRI-γ association increases Mincle expression and enhances phagocytosis of antibody-coated beads. Flow cytometry, co-immunoprecipitation, biochemical analysis, phagocytosis assay European journal of immunology High 23921530
2013 Mincle activation by TDM/TDB induces recognition through the CARD9 pathway, and recognition of TDM by Mincle partially explains the CARD9 requirement for pro-IL-1β expression. Peptidoglycan plus cord factor in mineral oil synergized to recapitulate Th17-promoting activity of CFA, with responses diminished in caspase-1- and CARD9-deficient mice, placing Mincle upstream of CARD9-dependent IL-1β transcription. Genetic epistasis (CARD9, caspase-1, ASC, NLRP3 KO mice), biochemical fractionation, adoptive transfer Journal of immunology (Baltimore, Md. : 1950) High 23630357
2014 Fonsecaea monophora engages CLR mincle to induce an E3 ubiquitin ligase Mdm2-dependent degradation pathway via Syk-CARD9-mediated PKB signaling, leading to loss of nuclear IRF1 activity and blocking IL12A transcription, thereby suppressing Th1 responses and promoting immune evasion. Genetic knockdown, reporter assays, signaling pathway inhibitors, chromatin/nucleosome remodeling assays Cell host & microbe High 24721577
2014 TDM-induced Mincle expression is dependent on Dectin-3-mediated NF-κB activation through the CARD9-BCL10-MALT1 complex. NF-κB but not NFAT binds the Mincle promoter. Dectin-3-deficient macrophages fail to upregulate Mincle in response to TDM. Genetic KO (Dectin-3, CARD9), NF-κB/NFAT inhibitors, chromatin immunoprecipitation at Mincle promoter The Journal of biological chemistry High 25202022
2014 Human mincle binds acylated trehalose derivatives via a mechanism similar to bovine mincle: one glucose of trehalose is ligated to the principal Ca2+-binding site; the second glucose contacts a secondary site; and acyl chains at 6-OH groups enhance affinity in a chain-length and hydrophobic-groove-dependent manner. Mutagenesis and synthetic analog binding studies showed the available crystal structure of human mincle CRD is not in the fully active conformation. Site-directed mutagenesis of human mincle, binding studies with synthetic TDM analogs Glycobiology High 25028392
2015 MCL interacts with Mincle through its stalk region to promote Mincle surface expression. MCL-deficient BMDCs show reduced Mincle protein (not mRNA) after stimulation. MCL transgenic mice show enhanced Mincle surface expression. A hydrophobic repeat in MCL stalk is required; substitution of four hydrophobic residues (MCL4S) abolishes the function, and MCL4S fails to restore TDM responses in MCL-deficient cells. Co-immunoprecipitation, domain swap/mutagenesis, transgenic and KO mice, flow cytometry for surface expression Journal of immunology (Baltimore, Md. : 1950) High 25888641
2015 Human Mincle binds cholesterol crystals (but not murine Mincle) and triggers innate immune responses including pro-inflammatory cytokine production. Purified cholesterol in plate-coated and crystallized forms activates hMincle-expressing reporter cells; anti-human Mincle antibody inhibits this response in human dendritic cells. Reporter cell assays, MS lipid identification, antibody blockade, transfection of murine macrophages with hMincle The Journal of biological chemistry High 26296894
2016 Mincle signaling in macrophages inhibits cholesterol efflux and induces a Syk-mediated endoplasmic reticulum stress response (dependent on Chop and Ire1a), leading to proinflammatory mediator and growth factor induction. Clec4e-/- bone marrow transplantation into Ldlr-/- mice reduces lipid accumulation, ER stress, macrophage inflammation and proliferation, and significantly limits atherosclerosis. Bone marrow chimera, Clec4e-/- genetic KO, in vitro macrophage assays, Syk inhibition, Chop/Ire1a/Atf3 KO Circulation High 27587433
2016 Leishmania triggers a Mincle-dependent inhibitory ITAM (ITAMi) configuration characterized by SHP1 coupling to the FcRγ chain, impairing dendritic cell activation and adaptive immunity. Mincle-deficient mice had milder pathology and lower parasite burdens. Selective loss of SHP1 in CD11c+ cells phenocopied enhanced adaptive immunity to Leishmania. Mincle-deficient mice, conditional SHP1 KO in CD11c+ cells, signaling analysis (SHP1-FcRγ coupling), parasite burden quantification Immunity High 27742545
2016 Mincle is essential for maintaining the M1 macrophage phenotype through Syk signaling. Mincle expression in macrophages is regulated by TLR4/NF-κB signaling; NF-κB/p65 binds the Mincle promoter in LPS-primed macrophages. Mincle knockdown or Syk inhibition suppresses LPS-induced IL-1β, MCP-1, and iNOS expression. Adoptive transfer of Mincle+ M1 macrophages promotes cisplatin-induced renal inflammation, prevented by Mincle knockdown. Mincle knockdown, Syk inhibitor, NF-κB/p65 ChIP at Mincle promoter, adoptive transfer, in vivo AKI model Kidney international High 28017324
2016 Mincle is the key switch for macrophage transition from cytokine expression to high nitric oxide production during mycobacterial infection. Beyond stimulating TLR-mediated transcription, Mincle enhances translation of key genes for nitric oxide synthesis through p38 and eIF5A hypusination, leading to granuloma resolution. Thus Mincle has dual transcriptional and translational regulatory functions. Mincle-deficient macrophages, p38 inhibitors, eIF5A hypusination assays, translation reporter assays, murine granuloma model Nature communications High 27089465
2016 Necroptosis-induced cytoplasmic SAP130 (a subunit of the histone deacetylase complex) in pancreatic ductal adenocarcinoma is sensed by Mincle on tumor-infiltrating myeloid cells, promoting oncogenesis and macrophage-induced immune suppression. Mincle deletion protected against PDA and reprogrammed the tumor microenvironment by releasing T cells into anti-tumor activity. Mincle-/- and RIP3-/- mouse models of PDA, SAP130 cytoplasmic expression analysis, adoptive transfer, T cell depletion experiments Nature High 27049944
2016 IRAKM Myddosome (formed at low LPS concentrations reflecting pathophysiological levels) mediates up-regulation of Mincle in macrophages. Mincle then senses SAP130 (released by ethanol-damaged hepatocytes), and SAP130 plus LPS synergistically activate inflammatory responses including inflammasome activation, contributing to alcoholic liver disease. IRAKM-/- and Mincle-/- mice, bone marrow-derived macrophage ex vivo assays, ethanol feeding model, inflammasome activation assays Hepatology (Baltimore, Md.) High 27628766
2016 C/EBPβ is a central transcriptional hub for Mincle expression and inflammatory gene induction in response to TDB/TDM. C/EBPβ-deficient macrophages nearly completely lose TDB/TDM responsiveness, partly because they fail to upregulate Mincle; retroviral rescue of Mincle expression restores Egr1 but not G-CSF induction, indicating additional C/EBPβ-dependent targets. HIF1α (induced by TDB/TDM in a C/EBPβ-dependent manner) controls Nos2 expression. C/EBPβ-/- and HIF1α-deficient macrophages/DCs, retroviral Mincle rescue, microarray, Syk phosphorylation assays Journal of immunology (Baltimore, Md. : 1950) High 25156364
2016 Microbial stimulation triggers Mincle expression through the MyD88 pathway without requiring MCL. MCL is constitutively expressed but retained intracellularly until Mincle is induced, whereupon Mincle and MCL form heterodimers that translocate to the cell surface ('two-step' model). MyD88-/- and MCL-/- macrophages, surface vs. intracellular protein localization by flow cytometry, heterodimer co-IP Microbes and infection High 27005451
2017 β-glucosylceramide (GlcCer), a ubiquitous intracellular metabolite, is an endogenous Mincle ligand released from damaged cells. Synthetic β-GlcCer activates myeloid cells and induces inflammatory cytokines in a Mincle-dependent manner. Enhanced sterile inflammation in hematopoietic GBA1-deficient mice (in which β-GlcCer accumulates) is ameliorated in Mincle-deficient background, establishing a physiological GlcCer-Mincle axis. Lipid fractionation, mass spectrometry, NMR, synthetic ligand, Mincle-/- cells and mice, GBA1/Mincle double-KO Proceedings of the National Academy of Sciences of the United States of America High 28373578
2017 Cholesterol sulfate is selectively recognized by Mincle (Clec4e) and causes secretion of proinflammatory mediators. Mincle is strongly upregulated in response to skin damage, and its absence significantly suppresses allergic contact dermatitis magnitude (ear thickness, myeloid infiltration, cytokines). Reporter cell assay, Mincle-/- mouse model of allergic contact dermatitis, in vivo cholesterol sulfate injection Proceedings of the National Academy of Sciences of the United States of America High 28292894
2017 Glycerol monomycolate (GroMM) is a ligand for human Mincle but not mouse Mincle. Domain-swap chimeras confirmed that the ectodomain of hMincle is required. Site-directed mutagenesis identified amino acid residues at positions 174-176 and 195-196 as critical for GroMM recognition. hMincle transgenic/mMincle-KO macrophages responded to GroMM with inflammatory cytokine production, while mMincle+ macrophages did not. Domain-swap chimeras, site-directed mutagenesis, reporter cell assays, hMincle transgenic/mMincle-KO mice The Journal of biological chemistry High 24733387
2017 The fine structure of fatty acids (including chain branching) plays a key role in glycolipid binding to the Mincle CRD. Glucose and mannose esterified at O-6 with a synthetic α-ramified 32-carbon fatty acid show agonist activity similar to TDM. Mincle-dependent proinflammatory cytokine production in primary human and murine cells was confirmed with these analogs. Chemical synthesis, molecular dynamics simulations, protein mutagenesis, reporter cell assays, primary cell stimulation, in vivo immunization Proceedings of the National Academy of Sciences of the United States of America High 28223515
2016 Binding studies reveal that the apparent affinity of mincle for hydrophobic ligands correlates with overall size rather than specific structural preference. X-ray crystallography of an extended extracellular domain of mincle (beyond the minimal CRD) and mutagenesis confirm three Ca2+-binding sites and multiple hydrophobic surface contacts for acyl chain binding. X-ray crystallography, binding assays with synthetic trehalose mimics, site-directed mutagenesis The Journal of biological chemistry High 27542410
2018 Lipoteichoic acid anchor monoglucosyldiacylglycerol (MGDG) produced by Group A Streptococcus is recognized by Mincle, triggering CARD9 pathway-dependent production of inflammatory cytokines, iNOS, and reactive oxygen species. Mincle-deficient mice exhibit impaired cytokine production, severe bacteremia, and rapid lethality after GAS infection. Diglucosyldiacylglycerol, another GAS ligand, interfered with MGDG-induced activation. Reporter cell assay with purified ligands, Mincle-/- mice (in vivo infection model), gene expression analysis, CARD9 pathway inhibition Proceedings of the National Academy of Sciences of the United States of America High 30352847
2018 CD11b acts as a critical negative regulator of Mincle signaling. Mincle activation by mycobacterial components induces formation of a Mincle-CD11b signaling complex. Activated CD11b recruits Lyn, SIRPα, and SHP1, which dephosphorylate Syk to inhibit Mincle-mediated inflammation. CD11b-deficient mice show hyperinflammation following mycobacterial infection. CD11b-/- macrophages and mice, co-immunoprecipitation, Syk dephosphorylation assay, Lyn activator MLR1023 Experimental & molecular medicine High 29400702
2019 The Mincle-Syk axis in dendritic cells senses mucosal-resident commensals in Peyer's patches, triggers IL-6 and IL-23p19 expression, and thereby regulates intestinal Th17 and ILC3 function. Mincle-deficient or DC-specific Syk-deficient mice have impaired intestinal RegIIIγ and IgA production and increased systemic microbial translocation, leading to liver inflammation and deregulated lipid metabolism. Mincle-/- mice, CD11c-specific Syk conditional KO mice, intestinal immune profiling, microbiota sensing assays Immunity High 30709742
2019 CLEC4E (Mincle) signaling in macrophages activates MYD88, PI3K, STAT1, and RELA/NF-κB, increases lysosome biogenesis, and induces macroautophagy through MYD88. In autophagy-deficient (Atg5-KO or Becn1-knockdown) macrophages, Mtb survival is elevated. CLEC4E combined with TLR4 agonist (C4.T4) restricts Mtb growth through autophagy. Atg5-KO and Becn1-knockdown macrophages, autophagy flux assays, lysosome biogenesis markers, in vivo mouse and guinea pig infection Autophagy High 31462144
2020 Mincle senses renal tubular cell death via β-glucosylceramide as an endogenous ligand; free cholesterol markedly enhances β-glucosylceramide agonism on Mincle. Mincle-deficient mice are protected against tissue damage and kidney atrophy after ischemia-reperfusion injury. β-glucosylceramide and free cholesterol accumulate in dead renal tubules in proximity to Mincle-expressing macrophages, where Mincle inhibits dead-cell clearance. Mincle-/- mice (IRI model), lipophilic extract fractionation, mass spectrometry identification of β-GlcCer, functional reporter assays, histological co-localization The Journal of experimental medicine High 32797195
2020 The Mincle/Syk/NF-κB signaling circuit is essential for maintaining pro-tumoral activities of tumor-associated macrophages (TAM). Cancer cells induce Mincle expression in bone marrow-derived macrophages, and Mincle silencing promotes M1-like phenotypes. Ultrasound microbubble-mediated tumor-specific Mincle silencing blocked Mincle/Syk/NF-κB signaling and TAM-driven cancer progression in syngeneic mouse models. Single-cell RNA-seq, Mincle siRNA knockdown, adoptive transfer into NOD/SCID mice, syngeneic lung/melanoma models, ultrasound-mediated gene transfer Cancer immunology research High 32532809
2020 Mincle/Syk signaling in macrophages promotes intestinal mucosal inflammation in Crohn's disease by inducing macrophage pyroptosis and MAPK-dependent chemokine production to recruit neutrophils. Mincle-/- mice and Syk inhibitor treatment ameliorate experimental colitis by reducing macrophage pyroptosis. Mincle-/- mice in colitis model, Syk pharmacological inhibition, Mincle agonist, ex vivo BMDM pyroptosis assays Journal of Crohn's & colitis High 32333776
2021 Peroxiredoxin 1 (Prdx1) is a novel DAMP that binds Mincle to initiate macrophage-mediated AKI. Prdx1 upregulates Mincle and the Syk system; Mincle knockdown abolishes Prdx1-induced activated Syk and downstream NF-κB signaling and M1 polarization. Prdx1-/- mice are protected from AKI, and protection is reversed by recombinant Prdx1. Prdx1-/- mice, Mincle knockdown in macrophages, co-IP (Prdx1-Mincle interaction), Syk phosphorylation assays, recombinant protein rescue Kidney international High 37164261
2021 SAP130 released from damaged tubular cells drives necroinflammation via a miRNA-219c-3p/Mincle-dependent mechanism. miR-219c-3p binds the Mincle 3'-UTR to inhibit Mincle translation; lentivirus-mediated renal miR-219c-3p overexpression blunts Mincle expression, macrophage infiltration, and inflammation in UUO mice. SAP130 administration, Mincle-/- mice, miRNA 3'-UTR reporter assay, lentiviral miR-219c-3p overexpression in vivo Cell death & disease High 34556635
2022 Mincle has a T cell-intrinsic role in TH17-mediated CNS inflammation. Dying cells release β-glucosylceramide during inflammation, which serves as a natural ligand for Mincle on TH17 cells. Mincle ligand engagement induces ASC-NLRP3 inflammasome activation leading to Caspase8-dependent IL-1β production, driving TH17 cell proliferation via an autocrine loop. Mincle genomic deletion specifically in T cells impairs TH17- but not TH1-mediated EAE. T cell-specific Mincle-/- mice, NLRP3/ASC inflammasome assays, Caspase-8 inhibition, β-GlcCer synthesis inhibition, EAE model Nature communications High 35504893
2012 TDM-induced Mincle signaling on neutrophils increases cell adherence by enhancing F-actin polymerization and CD11b/CD18 surface expression, dependent on Src, Syk, and MEK kinases. Neutrophils are recruited during early TDM-induced granuloma formation, and Mincle expression on neutrophils is required for infiltration at TDM-challenged sites. Mincle-/- mice, neutrophil depletion, kinase inhibitors (Src, Syk, MEK), F-actin polymerization assays, CD11b/CD18 flow cytometry PLoS pathogens High 22496642
2017 TDM recruits Mincle during FcγR-mediated phagocytosis and modulates phagosome maturation through SHP-1 and FcγRIIB, indicating inhibitory downstream signaling of Mincle during phagosome formation. This provides a mechanism for TDM-mediated virulence. IgG-opsonized bead assays with TDM coating, phagosome maturation assays, SHP-1 and FcγRIIB genetic/pharmacological inhibition PloS one High 28384255
2016 Clec4e (Mincle) in the CNS (specifically in perivascular macrophages, not in microglia or neurons) exacerbates neuronal loss following ischemic stroke. Bone marrow chimera experiments revealed that CNS-resident rather than recruited immune cell Mincle drives poor outcomes after transient MCAO. Mincle-/- mice (MCAO, spinal cord injury, heart/gut ischemia models), bone marrow chimeras, leukocyte infiltration and infarct size analysis Journal of cerebral blood flow and metabolism High 27492949
2013 Mincle and Syk are upregulated after cerebral ischemia. Piceatannol (a Syk inhibitor) reduces infarct volume, suppresses phospho-Syk, MMP9, and ICAM-1 expression, and upregulates Claudin5, indicating Mincle/Syk signaling participates in post-ischemic inflammation. Mincle/SAP130/pSyk immunohistochemistry in mouse and human brain, Syk inhibitor piceatannol in mouse MCAO model Scientific reports Medium 24212132
2021 Clec4e (Mincle) expression is increased in vasculature, cardiac myocytes, and infiltrating leukocytes after myocardial ischemia-reperfusion injury. Loss of Clec4e signaling reduces acute cardiac injury, neutrophil infiltration, and infarct size, and improves left ventricular structural and functional remodeling at 4 weeks. CNS-resident rather than recruited cell Mincle contributes (bone marrow chimera in stroke model referenced). Clec4e-/- mice in porcine and murine IRI models, transcriptomic profiling, LV functional assessment by imaging JACC. Basic to translational science High 34466750
2019 Mincle-Syk axis in dendritic cells senses gut microbiota; microbiota dysbiosis reduces lung Mincle expression on DCs, impairing their ability to activate naïve CD4 T cells and increasing Mtb susceptibility. TDB (Mincle ligand) administration rescues DC function and T cell response. Antibiotic-induced dysbiosis in mice, Mincle expression on lung DCs, DC-T cell co-culture assays, TDB rescue in vivo Frontiers in immunology Medium 31231363
2017 Mincle recognizes the glycosylated surface (S)-layer of Tannerella forsythia in a specific, Ca2+-dependent manner via recombinant Mincle-Fc fusion protein binding. Mincle knockdown in macrophages reduces both pro- and anti-inflammatory cytokine secretion in response to T. forsythia and its S-layer. Recombinant Mincle-Fc binding assay, Mincle knockdown macrophages, cytokine measurements PloS one Medium 28264048
2016 SAP130 and Mincle mediate cross-talk between neuronal necroptosis and microglial immunity after SAH-related injury. Albumin binds microglial Mincle receptor directly, retarding Mincle/Syk/IL-1β signaling and attenuating SAP130-induced Mincle upregulation. The anti-inflammatory effect of albumin is similar to Mincle genetic knockdown. Co-IP (albumin-Mincle binding), Mincle siRNA knockdown in BV-2 cells, in vivo SAH rat model with albumin treatment Brain, behavior, and immunity Medium 27845194
2020 C-type lectin receptors Mcl and Mincle, expressed in CNS myeloid cells, are crucial for pathogenesis of EAE (MS model). In vivo silencing of Mcl and Mincle or SAP130 blockade reduces T cell recruitment and reactivation to pathogenic Th17/GM-CSF phenotype. SAP130-Mincle signaling in the CNS is the critical driver. In vivo Mcl/Mincle siRNA silencing, SAP130 blockade, congenic rats with lower Mcl/Mincle expression, EAE model, human MS lesion analysis The Journal of clinical investigation High 31725411
2016 Glucosyl-diacylglycerol (Glc-DAG) of Streptococcus pneumoniae is identified as a Mincle ligand. Glc-DAG activates Mincle reporter cells and stimulates cytokine release from alveolar macrophages of WT but not Mincle-KO mice. Mincle deficiency increases bacterial loads and decreases survival in pneumococcal pneumonia, normalized by WT hematopoietic reconstitution. Reporter cell assay with purified Glc-DAG, Mincle-KO mice, bone marrow chimera PLoS pathogens High 27923071
2024 TEC ferroptosis in sepsis AKI triggers SAP130 release, which promotes M1 macrophage polarization through Mincle/Syk/NF-κB signaling. M1 macrophages in turn aggravate TEC ferroptosis. Neutralizing SAP130 or inhibiting Mincle expression blunts this feed-forward loop. Ferroptosis inhibitor Fer-1 in CLP/LPS AKI models, co-culture systems, SAP130 neutralizing antibody, Mincle knockdown, M1 polarization flow cytometry International immunopharmacology Medium 38320352

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Direct recognition of the mycobacterial glycolipid, trehalose dimycolate, by C-type lectin Mincle. The Journal of experimental medicine 611 20008526
2008 Mincle is an ITAM-coupled activating receptor that senses damaged cells. Nature immunology 564 18776906
2016 The necrosome promotes pancreatic oncogenesis via CXCL1 and Mincle-induced immune suppression. Nature 518 27049944
2010 Cutting edge: Mincle is essential for recognition and adjuvanticity of the mycobacterial cord factor and its synthetic analog trehalose-dibehenate. Journal of immunology (Baltimore, Md. : 1950) 385 20164423
2009 C-type lectin Mincle is an activating receptor for pathogenic fungus, Malassezia. Proceedings of the National Academy of Sciences of the United States of America 342 19171887
2019 Microbiota Sensing by Mincle-Syk Axis in Dendritic Cells Regulates Interleukin-17 and -22 Production and Promotes Intestinal Barrier Integrity. Immunity 181 30709742
2016 The pattern recognition receptor, Mincle, is essential for maintaining the M1 macrophage phenotype in acute renal inflammation. Kidney international 146 28017324
2017 Intracellular metabolite β-glucosylceramide is an endogenous Mincle ligand possessing immunostimulatory activity. Proceedings of the National Academy of Sciences of the United States of America 138 28373578
2013 Structural analysis for glycolipid recognition by the C-type lectins Mincle and MCL. Proceedings of the National Academy of Sciences of the United States of America 131 24101491
2013 The Mincle-activating adjuvant TDB induces MyD88-dependent Th1 and Th17 responses through IL-1R signaling. PloS one 117 23308247
2012 Neutrophils Promote Mycobacterial Trehalose Dimycolate-Induced Lung Inflammation via the Mincle Pathway. PLoS pathogens 117 22496642
2014 Fungal engagement of the C-type lectin mincle suppresses dectin-1-induced antifungal immunity. Cell host & microbe 113 24721577
2014 MCL and Mincle: C-Type Lectin Receptors That Sense Damaged Self and Pathogen-Associated Molecular Patterns. Frontiers in immunology 110 25002863
2015 Human Mincle Binds to Cholesterol Crystals and Triggers Innate Immune Responses. The Journal of biological chemistry 107 26296894
2013 Cord factor and peptidoglycan recapitulate the Th17-promoting adjuvant activity of mycobacteria through mincle/CARD9 signaling and the inflammasome. Journal of immunology (Baltimore, Md. : 1950) 107 23630357
2019 Quercetin protects against cisplatin-induced acute kidney injury by inhibiting Mincle/Syk/NF-κB signaling maintained macrophage inflammation. Phytotherapy research : PTR 102 31497913
2013 Mechanism for recognition of an unusual mycobacterial glycolipid by the macrophage receptor mincle. The Journal of biological chemistry 102 23960080
2014 C-type lectin receptor dectin-3 mediates trehalose 6,6'-dimycolate (TDM)-induced Mincle expression through CARD9/Bcl10/MALT1-dependent nuclear factor (NF)-κB activation. The Journal of biological chemistry 101 25202022
2020 Isoliquiritigenin Attenuates UUO-Induced Renal Inflammation and Fibrosis by Inhibiting Mincle/Syk/NF-Kappa B Signaling Pathway. Drug design, development and therapy 99 32341639
2018 Curcumin relieved cisplatin-induced kidney inflammation through inhibiting Mincle-maintained M1 macrophage phenotype. Phytomedicine : international journal of phytotherapy and phytopharmacology 95 30599909
2015 C-Type Lectin Receptor MCL Facilitates Mincle Expression and Signaling through Complex Formation. Journal of immunology (Baltimore, Md. : 1950) 95 25888641
2017 Rational design of adjuvants targeting the C-type lectin Mincle. Proceedings of the National Academy of Sciences of the United States of America 90 28223515
2016 Human albumin attenuates excessive innate immunity via inhibition of microglial Mincle/Syk signaling in subarachnoid hemorrhage. Brain, behavior, and immunity 90 27845194
2013 Mincle, the receptor for mycobacterial cord factor, forms a functional receptor complex with MCL and FcεRI-γ. European journal of immunology 90 23921530
2016 Age-Specific Adjuvant Synergy: Dual TLR7/8 and Mincle Activation of Human Newborn Dendritic Cells Enables Th1 Polarization. Journal of immunology (Baltimore, Md. : 1950) 83 27793997
2016 Leishmania Uses Mincle to Target an Inhibitory ITAM Signaling Pathway in Dendritic Cells that Dampens Adaptive Immunity to Infection. Immunity 82 27742545
2009 Mincle is a long sought receptor for mycobacterial cord factor. The Journal of experimental medicine 82 20008525
2019 Gut Microbiota Regulates Mincle Mediated Activation of Lung Dendritic Cells to Protect Against Mycobacterium tuberculosis. Frontiers in immunology 81 31231363
2015 Contribution of MINCLE-SYK Signaling to Activation of Primary Human APCs by Mycobacterial Cord Factor and the Novel Adjuvant TDB. Journal of immunology (Baltimore, Md. : 1950) 80 26202982
2008 Human and mouse macrophage-inducible C-type lectin (Mincle) bind Candida albicans. Glycobiology 80 18509109
2017 Receptor Mincle promotes skin allergies and is capable of recognizing cholesterol sulfate. Proceedings of the National Academy of Sciences of the United States of America 74 28292894
2018 Mincle: 20 years of a versatile sensor of insults. International immunology 73 29726997
2013 Involvement of Mincle and Syk in the changes to innate immunity after ischemic stroke. Scientific reports 71 24212132
2016 Necrotic Cell Sensor Clec4e Promotes a Proatherogenic Macrophage Phenotype Through Activation of the Unfolded Protein Response. Circulation 70 27587433
2019 Induction of autophagy through CLEC4E in combination with TLR4: an innovative strategy to restrict the survival of Mycobacterium tuberculosis. Autophagy 69 31462144
2013 Protective role of Mincle in bacterial pneumonia by regulation of neutrophil mediated phagocytosis and extracellular trap formation. The Journal of infectious diseases 68 24353272
2014 Glycerol monomycolate is a novel ligand for the human, but not mouse macrophage inducible C-type lectin, Mincle. The Journal of biological chemistry 67 24733387
2016 Binding Sites for Acylated Trehalose Analogs of Glycolipid Ligands on an Extended Carbohydrate Recognition Domain of the Macrophage Receptor Mincle. The Journal of biological chemistry 66 27542410
2016 IRAKM-Mincle axis links cell death to inflammation: Pathophysiological implications for chronic alcoholic liver disease. Hepatology (Baltimore, Md.) 62 27628766
2012 Role of Mincle in alveolar macrophage-dependent innate immunity against mycobacterial infections in mice. Journal of immunology (Baltimore, Md. : 1950) 61 22869905
2023 Peroxiredoxin 1 aggravates acute kidney injury by promoting inflammation through Mincle/Syk/NF-κB signaling. Kidney international 60 37164261
2020 The Mincle/Syk/NF-κB Signaling Circuit Is Essential for Maintaining the Protumoral Activities of Tumor-Associated Macrophages. Cancer immunology research 59 32532809
2017 Sensing Lipids with Mincle: Structure and Function. Frontiers in immunology 59 29230225
2014 Differential control of Mincle-dependent cord factor recognition and macrophage responses by the transcription factors C/EBPβ and HIF1α. Journal of immunology (Baltimore, Md. : 1950) 58 25156364
2016 C-type Lectin Mincle Recognizes Glucosyl-diacylglycerol of Streptococcus pneumoniae and Plays a Protective Role in Pneumococcal Pneumonia. PLoS pathogens 57 27923071
2016 Mincle-mediated translational regulation is required for strong nitric oxide production and inflammation resolution. Nature communications 56 27089465
2013 Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis. Frontiers in immunology 54 23355839
2020 C-type lectin Mincle mediates cell death-triggered inflammation in acute kidney injury. The Journal of experimental medicine 52 32797195
2012 Mincle polarizes human monocyte and neutrophil responses to Candida albicans. Immunology and cell biology 51 22641025
2015 Fonsecaea pedrosoi-induced Th17-cell differentiation in mice is fostered by Dectin-2 and suppressed by Mincle recognition. European journal of immunology 49 26140582
2015 Corynomycolic acid-containing glycolipids signal through the pattern recognition receptor Mincle. Chemical communications (Cambridge, England) 45 25714652
2020 Mincle/Syk Signalling Promotes Intestinal Mucosal Inflammation Through Induction of Macrophage Pyroptosis in Crohn's Disease. Journal of Crohn's & colitis 44 32333776
2017 The Interaction of Pneumocystis with the C-Type Lectin Receptor Mincle Exerts a Significant Role in Host Defense against Infection. Journal of immunology (Baltimore, Md. : 1950) 44 28298521
2015 Induction of Mincle by Helicobacter pylori and consequent anti-inflammatory signaling denote a bacterial survival strategy. Scientific reports 43 26456705
2014 Defining the conformation of human mincle that interacts with mycobacterial trehalose dimycolate. Glycobiology 43 25028392
2015 The C-type lectin receptor Mincle binds to Streptococcus pneumoniae but plays a limited role in the anti-pneumococcal innate immune response. PloS one 42 25658823
2018 Lipoteichoic acid anchor triggers Mincle to drive protective immunity against invasive group A Streptococcus infection. Proceedings of the National Academy of Sciences of the United States of America 41 30352847
2021 Artesunate relieves acute kidney injury through inhibiting macrophagic Mincle-mediated necroptosis and inflammation to tubular epithelial cell. Journal of cellular and molecular medicine 40 34337860
2016 Trehalose diester glycolipids are superior to the monoesters in binding to Mincle, activation of macrophages in vitro and adjuvant activity in vivo. Innate immunity 40 27252171
2016 An atypical role for the myeloid receptor Mincle in central nervous system injury. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 40 27492949
2015 Mycobacterial receptor, Clec4d (CLECSF8, MCL), is coregulated with Mincle and upregulated on mouse myeloid cells following microbial challenge. European journal of immunology 40 26558717
2017 M1 macrophage triggered by Mincle leads to a deterioration of acute kidney injury. Kidney international 39 28202166
2017 The Mincle ligand trehalose dibehenate differentially modulates M1-like and M2-like macrophage phenotype and function via Syk signaling. Immunity, inflammation and disease 39 28722316
2010 Self and nonself recognition through C-type lectin receptor, Mincle. Self/nonself 38 21487505
2017 Trehalose dimycolate interferes with FcγR-mediated phagosome maturation through Mincle, SHP-1 and FcγRIIB signalling. PloS one 37 28384255
2016 Mincle Signaling Promotes Con A Hepatitis. Journal of immunology (Baltimore, Md. : 1950) 37 27559045
2014 Macrophage-inducible C-type lectin Mincle-expressing dendritic cells contribute to control of splenic Mycobacterium bovis BCG infection in mice. Infection and immunity 37 25332121
2021 BAY61‑3606 attenuates neuroinflammation and neurofunctional damage by inhibiting microglial Mincle/Syk signaling response after traumatic brain injury. International journal of molecular medicine 36 34751408
2018 Microglial Mincle receptor in the PVN contributes to sympathetic hyperactivity in acute myocardial infarction rat. Journal of cellular and molecular medicine 35 30353660
2016 Mincle-mediated anti-inflammatory IL-10 response counter-regulates IL-12 in vitro. Innate immunity 35 26939595
2015 Mycobacterium tuberculosis β-gentiobiosyl diacylglycerides signal through the pattern recognition receptor Mincle: total synthesis and structure activity relationships. Chemical communications (Cambridge, England) 35 26310657
2017 Toll-Like Receptor 2 and Mincle Cooperatively Sense Corynebacterial Cell Wall Glycolipids. Infection and immunity 34 28483856
2016 Total synthesis of a cyclopropane-fatty acid α-glucosyl diglyceride from Lactobacillus plantarum and identification of its ability to signal through Mincle. Chemical communications (Cambridge, England) 34 27533919
2021 SAP130 released by damaged tubule drives necroinflammation via miRNA-219c/Mincle signaling in acute kidney injury. Cell death & disease 33 34556635
2020 Astragalus propinquus Schischkin and Panax notoginseng (A&P) compound relieved cisplatin-induced acute kidney injury through inhibiting the mincle maintained macrophage inflammation. Journal of ethnopharmacology 33 32004631
2015 The natural product brartemicin is a high affinity ligand for the carbohydrate-recognition domain of the macrophage receptor mincle. MedChemComm 33 25893085
2021 Clec4e-Receptor Signaling in Myocardial Repair After Ischemia-Reperfusion Injury. JACC. Basic to translational science 32 34466750
2017 Macrophage inducible C-type lectin (Mincle) recognizes glycosylated surface (S)-layer of the periodontal pathogen Tannerella forsythia. PloS one 31 28264048
2019 The CARD9-Associated C-Type Lectin, Mincle, Recognizes La Crosse Virus (LACV) but Plays a Limited Role in Early Antiviral Responses against LACV. Viruses 30 30917612
2021 S-Layer From Lactobacillus brevis Modulates Antigen-Presenting Cell Functions via the Mincle-Syk-Card9 Axis. Frontiers in immunology 29 33732234
2019 The pattern recognition receptors dectin-2, mincle, and FcRγ impact the dynamics of phagocytosis of Candida, Saccharomyces, Malassezia, and Mucor species. PloS one 29 31393930
2024 SAP130 released by ferroptosis tubular epithelial cells promotes macrophage polarization via Mincle signaling in sepsis acute kidney injury. International immunopharmacology 28 38320352
2020 C-type lectin receptors Mcl and Mincle control development of multiple sclerosis-like neuroinflammation. The Journal of clinical investigation 28 31725411
2008 Sensing necrosis with Mincle. Nature immunology 28 18800160
2018 CD209a Synergizes with Dectin-2 and Mincle to Drive Severe Th17 Cell-Mediated Schistosome Egg-Induced Immunopathology. Cell reports 27 29386115
2012 Mincle and human B cell function. Journal of autoimmunity 27 22698596
2022 TH17 cells promote CNS inflammation by sensing danger signals via Mincle. Nature communications 26 35504893
2018 The Mycobacterial Adjuvant Analogue TDB Attenuates Neuroinflammation via Mincle-Independent PLC-γ1/PKC/ERK Signaling and Microglial Polarization. Molecular neurobiology 26 29876879
2017 Mincle inhibits neutrophils and macrophages apoptosis in A. fumigatus keratitis. International immunopharmacology 26 28888778
2018 Synthesis of Branched Trehalose Glycolipids and Their Mincle Agonist Activity. The Journal of organic chemistry 25 29781274
2016 Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation. Microbes and infection 25 27005451
2012 Silencing of renal DNaseI in murine lupus nephritis imposes exposure of large chromatin fragments and activation of Toll like receptors and the Clec4e. PloS one 25 22479529
2023 Macrophages mediate psoriasis via Mincle-dependent mechanism in mice. Cell death discovery 23 37117184
2019 S-Layer Glycoprotein From Lactobacillus kefiri Exerts Its Immunostimulatory Activity Through Glycan Recognition by Mincle. Frontiers in immunology 23 31297112
2019 Species-Specific Structural Requirements of Alpha-Branched Trehalose Diester Mincle Agonists. Frontiers in immunology 22 30873180
2018 Integrin CD11b negatively regulates Mincle-induced signaling via the Lyn-SIRPα-SHP1 complex. Experimental & molecular medicine 22 29400702
2016 Stat6-Dependent Inhibition of Mincle Expression in Mouse and Human Antigen-Presenting Cells by the Th2 Cytokine IL-4. Frontiers in immunology 22 27790218
2021 Orientia tsutsugamushi selectively stimulates the C-type lectin receptor Mincle and type 1-skewed proinflammatory immune responses. PLoS pathogens 21 34320039
2017 Immune transcriptome reveals the mincle C-type lectin receptor acts as a partial replacement for TLR4 in lipopolysaccharide-mediated inflammatory response in barramundi (Lates calcarifer). Molecular immunology 21 28095348
2020 6,6'-Aryl trehalose analogs as potential Mincle ligands. Bioorganic & medicinal chemistry 20 32616186