ArticleNature communications2023
C-type lectin receptor 2d forms homodimers and heterodimers with TLR2 to negatively regulate IRF5-mediated antifungal immunity.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
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- C-type lectin-like domain family 2 (CLEC2D) promotes proliferation and migration of breast cancer and serves as a poor prognostic factor.Breast cancer (Tokyo, Japan) · 2026Article
- The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026Review
- Subcellular glycan-mannose receptor binding kinetics correlate with myeloid cell function.Nature communications · 2025Article
- Emergence, function, and therapeutic strategies to target the PD-1/PD-L1 immune checkpoint during pathogenic fungal infections.Virulence · 2025Review
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- DC-SIGN (CD209)-mediated interactions between bacteria, lung cancer tissues, and macrophages promote cancer metastasis.Infectious agents and cancer · 2025Article
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- A secreted C-type lectin in Periplaneta americana functioning in antibacterial activity, innate immune signaling and leg regeneration.Frontiers in immunology · 2025Article
- Dust mite antigens endow dendritic cells with the capacity to induce a Th2 response by regulating their methylation profiles.Cell communication and signaling : CCS · 2024Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Innate immune signal transduction pathways to fungal infection: Components and regulation.Cell insight · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dimerization of C-type lectin receptors (CLRs) or Toll-like receptors (TLRs) can alter their ligand binding ability, thereby modulating immune responses. However, the possibilities and roles of dimerization between CLRs and TLRs remain unclear. Here we show that C-type lectin receptor-2d (CLEC2D) forms homodimers, as well as heterodimers with TLR2. Quantitative ligand binding assays reveal that both CLEC2D homodimers and CLEC2D/TLR2 heterodimers have a higher binding ability to fungi-derived β-glucans than TLR2 homodimers. Moreover, homo- or hetero-dimeric CLEC2D mediates β-glucan-induced ubiquitination and degradation of MyD88 to inhibit the activation of transcription factor IRF5 and subsequent IL-12 production. Clec2d-deficient female mice are resistant to infection with Candida albicans, a human fungal pathogen, owing to the increase of IL-12 production and subsequent generation of IFN-γ-producing NK cells. Together, these data indicate that CLEC2D forms homodimers or heterodimers with TLR2, which negatively regulate antifungal immunity through suppression of IRF5-mediated IL-12 production. These homo- and hetero-dimers of CLEC2D and TLR2 provide an example of receptor dimerization to regulate host innate immunity against microbial infections.
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