ArticleScientific reports2019
Essential roles of C-type lectin Mincle in induction of neuropathic pain in mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Spinal Mincle activation as a new model of neuroinflammation-associated neuropathic pain: comparison with spinal nerve ligation.The Korean journal of pain · 2026Article
- Small molecules as ligands in the tuning of immune regulatory receptors.Frontiers in immunology · 2025Review
- Article
- Lectin Receptors in Primary and Metastatic Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- A network pharmacology approach to predict potential targets and mechanisms of "Annals of medicine · 2022Article
- Host immune responses in the central nervous system during fungal infections.Immunological reviews · 2022Review
- AIP1 suppresses neovascularization by inhibiting the NOX4-induced NLRP3/NLRP6 imbalance in a murine corneal alkali burn model.Cell communication and signaling : CCS · 2022Article
- Role of Dectin-1 in peripheral nerve injury.Frontiers in cellular neuroscience · 2022Article
- Secreted C-type lectin regulation of neuromuscular junction synaptic vesicle dynamics modulates coordinated movement.Journal of cell science · 2021Article
- Proteomic Analysis of the Venom of JellyfishesMarine drugs · 2020Article
- C-Type Lectin-Like Receptors: Head or Tail in Cell Death Immunity.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence indicates that pattern recognition receptors (PRRs) are involved in neuropathic pain after peripheral nerve injury (PNI). While a significant number of studies support an association between neuropathic pain and the innate immune response mediated through Toll-like receptors, a family of PRRs, the roles of other types of PRRs are largely unknown. In this study, we have focused on the macrophage-inducible C-type lectin (Mincle), a PRR allocated to the C-type lectin receptor family. Here, we show that Mincle is involved in neuropathic pain after PNI. Mincle-deficient mice showed impaired PNI-induced mechanical allodynia. After PNI, expression of Mincle mRNA was rapidly increased in the injured spinal nerve. Most Mincle-expressing cells were identified as infiltrating leucocytes, although the migration of leucocytes was also observed in Mincle-deficient mice. Furthermore, Mincle-deficiency affected the induction of genes, which are reported to contribute to neuropathic pain after PNI in the dorsal root ganglia and spinal dorsal horn. These results suggest that Mincle is involved in triggering sequential processes that lead to the pathogenesis of neuropathic pain.
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