ArticleThe American journal of pathology2020
Neurokinin-1 Receptor Antagonism Ameliorates Dry Eye Disease by Inhibiting Antigen-Presenting Cell Maturation and T Helper 17 Cell Activation.
Article in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- A transient receptor potential vanilloid 1-dependent corneal-trigeminal neuroinflammatory circuit promotes corneal neuropathy.Experimental & molecular medicine · 2026Article
- Tear neuropeptides are associated with clinical symptoms and signs of dry eye patients.Annals of medicine · 2025Article
- The Immunobiology of Dry Eye Disease: A Review of the Pathogenesis, Regulation and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Long-Term Clinical and Molecular Changes in Dry Eye Disease and Chronic Ocular Pain.International journal of molecular sciences · 2025Article
- The Role ofBiomolecules · 2025Review
- A Silk Fibroin Nanoparticle Hydrogel Loaded With NK1R Antagonist Has Synergistic Anti-Inflammatory and Reparative Effects on Dry Eye Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Anti-inflammatory effects of LCB 03-0110 on human corneal epithelial and murine T helper 17 cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Topical neurokinin-1 receptor antagonism ameliorates ocular pain and prevents corneal nerve degeneration in an animal model of dry eye disease.Pain reports · 2025Article
- Discovery of a novel thiophene carboxamide analogue as a highly potent and selective sphingomyelin synthase 2 inhibitor for dry eye disease therapy.Acta pharmaceutica Sinica. B · 2025Article
- Substance P regulates memory Th17 cell generation and maintenance in chronic dry eye disease.Journal of leukocyte biology · 2024Article
- IL-6 induces Treg dysfunction in desiccating stress-induced dry eye disease.Experimental eye research · 2024Article
- How does ocular graft-versus-host disease fit under the dry eye umbrella? A review.Clinical & experimental ophthalmology · 2024Review
- Multidimensional immunotherapy for dry eye disease: current status and future directions.Frontiers in ophthalmology · 2024Review
- Chronic Kidney Disease Has No Impact on Tear Film Substance P Concentration in Type 2 Diabetes.Biomedicines · 2023Article
- New insights into molecular signaling pathways and current advancements in prostate cancer diagnostics & therapeutics.Frontiers in oncology · 2023Review
- Therapeutic efficacy of topical blockade of substance P in experimental allergic red eye.The ocular surface · 2022Article
- Immunomodulatory Role of Neuropeptides in the Cornea.Biomedicines · 2022Review
- Skin codelivery of contact sensitizers and neurokinin-1 receptor antagonists integrated in microneedle arrays suppresses allergic contact dermatitis.The Journal of allergy and clinical immunology · 2022Article
- Modulating the tachykinin: Role of substance P and neurokinin receptor expression in ocular surface disorders.The ocular surface · 2022Review
- Corneal Epithelium-Derived Netrin-1 Alleviates Dry Eye Disease via Regulating Dendritic Cell Activation.Investigative ophthalmology & visual science · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Neuroinflammation plays an important role in the pathogenesis of ocular surface disease, including dry eye disease (DED), but little is known about the contribution of substance P (SP) to DED. In this study, we investigated the expression of SP at the ocular surface and evaluated its effect on maturation of antigen-presenting cells (APCs), the key cell component involved in the induction of type 17 helper T-cell (Th17) response in DED. The effect of topical blockade of SP signaling was further investigated using neurokinin-1 receptor (NK1R) inhibitors on APC maturation, Th17 cell activation, and disease severity in a mouse model of DED. The results demonstrate that SP is constitutively expressed at the ocular surface, and trigeminal ganglion neurons are the major source of SP in DED. SP derived from trigeminal ganglion enhanced the expression of major histocompatibility complex class II maturation marker by bone marrow-derived dendritic cells, an effect that is abrogated by blockade of SP signaling using NK1R antagonist spantide. Finally, using a well-established murine model of DED, topical treatment of DED mice with NK1R antagonists CP-99,994 and L-733,060 suppressed APC acquisition of major histocompatibility complex class II, reduced Th17 cell activity, and ameliorated DED severity. These findings are of translational value, as they suggest that antagonizing NK1R-mediated SP signaling may be an effective strategy in suppressing Th17-mediated ocular surface disease.
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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.