ArticleEuropean journal of immunology2016
Mycobacterial receptor, Clec4d (CLECSF8, MCL), is coregulated with Mincle and upregulated on mouse myeloid cells following microbial challenge.
Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- CAR design equips diverse immune cells with unique antigen-specific activation identities.Molecular therapy. Oncology · 2026Article
- Article
- Unravelling mechanisms regulating Mincle activation.Communications biology · 2026Review
- CLEC4D as an Effective Indicator for Assessing Severity of Illness in Critically Ill Patients: A Prospective Study.International journal of general medicine · 2026Article
- Proteomic, metabolomic and lipidomic profiles in community acquired pneumonia for differentiating viral and bacterial infections.Scientific reports · 2025Article
- Zebrafish use conserved CLR and TLR signaling pathways to respond to fungal PAMPs in zymosan.Developmental and comparative immunology · 2025Article
- The Dectin-1 and Dectin-2 clusters: C-type lectin receptors with fundamental roles in immunity.EMBO reports · 2024Review
- Zebrafish use conserved CLR and TLR signaling pathways to respond to fungal PAMPs in zymosan.bioRxiv : the preprint server for biology · 2024Article
- Differential Gene Expression Involved in Bone Turnover of Mice Expressing Constitutively Active TGFβ Receptor Type I.International journal of molecular sciences · 2024Article
- Quantitative proteomics reveals tissue-specific, infection-induced and species-specific neutrophil protein signatures.Scientific reports · 2024Article
- CLEC4D as a Novel Prognostic Marker Boosts the Proliferation and Migration of Gastric Cancer via the NF-κB/AKT Signaling Pathway.International journal of general medicine · 2024Article
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Human macrophage C-type lectin forms a heteromeric receptor complex with Mincle but not Dectin-2.Scandinavian journal of immunology · 2022Article
- Fungal-induced glycolysis in macrophages promotes colon cancer by enhancing innate lymphoid cell secretion of IL-22.The EMBO journal · 2021Article
- Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance toFrontiers in immunology · 2021Review
- Innate Immune Pattern Recognition Receptors of Mycobacterium tuberculosis: Nature and Consequences for Pathogenesis of Tuberculosis.Advances in experimental medicine and biology · 2021Article
- Differential expression of genes associated with T lymphocytes function in septic patients with hypoxemia challenge.Annals of translational medicine · 2019Article
- Recognition of DHN-melanin by a C-type lectin receptor is required for immunity to Aspergillus.Nature · 2018Article
- Pneumocystis and interactions with host immune receptors.PLoS pathogens · 2018Article
- Regulation of C-Type Lectin Receptor-Mediated Antifungal Immunity.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The C-type lectin receptor (CTLR), Clec4d (MCL, CLECSF8), is a member of the Dectin-2 cluster of CTLRs, which also includes the related receptors Mincle and Dectin-2. Like Mincle, Clec4d recognizes mycobacterial cord factor, trehalose dimycolate, and we recently demonstrated its key role in anti-mycobacterial immunity in mouse and man. Here, we characterized receptor expression in naïve mice, under inflammatory conditions, and during Mycobacterium bovis BCG infection using newly generated monoclonal antibodies. In naïve mice, Clec4d was predominantly expressed on myeloid cells within the peritoneal cavity, blood, and bone marrow. Unexpectedly, basal expression of Clec4d was very low on leukocytes in the lung. However, receptor expression was significantly upregulated on pulmonary myeloid cells during M. bovis BCG infection. Moreover, Clec4d expression could be strongly induced in vitro and in vivo by various microbial stimuli, including TLR agonists, but not exogenous cytokines. Notably, we show that Clec4d requires association with the signaling adaptor FcRγ and Mincle, but not Dectin-2, for surface expression. In addition, we provide evidence that Clec4d and Mincle, but not Dectin-2, are interdependently coregulated during inflammation and infection. These data show that Clec4d is an inducible myeloid-expressed CTLR in mice, whose expression is tightly linked to that of Mincle.
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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.