ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Retinal laser burn-induced neuropathy leads to substance P-dependent loss of ocular immune privilege.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Substance P induces sympathetic immune response in the contralateral eye after the first eye cataract surgery in type 2 diabetic patients.BMC ophthalmology · 2020Trial
- Loss of Pigment Epithelium Derived Factor Sensitizes C57BL/6J Mice to Light-Induced Retinal Damage.bioRxiv : the preprint server for biology · 2024Article
- Trigeminal nerve-derived substance P regulates limbal stem cells by the PI3K-AKT pathway.iScience · 2023Article
- FoxP3 expression by retinal pigment epithelial cells: transcription factor with potential relevance for the pathology of age-related macular degeneration.Journal of neuroinflammation · 2022Article
- The cornea IV immunology, infection, neovascularization, and surgery chapter 1: Corneal immunology.Experimental eye research · 2021Review
- The ocular surface immune system through the eyes of aging.The ocular surface · 2021Review
- "Corneal Nerves, CD11cFrontiers in immunology · 2021Review
- The Role of Retinal Pigment Epithelial Cells in Regulation of Macrophages/Microglial Cells in Retinal Immunobiology.Frontiers in immunology · 2021Review
- Corneal Nerve Ablation Abolishes Ocular Immune Privilege by Downregulating CD103 on T Regulatory Cells.Investigative ophthalmology & visual science · 2020Article
- Neurokinin-1 Receptor Antagonism Ameliorates Dry Eye Disease by Inhibiting Antigen-Presenting Cell Maturation and T Helper 17 Cell Activation.The American journal of pathology · 2020Article
- The Eye Sees Eye to Eye With the Immune System: The 2019 Proctor Lecture.Investigative ophthalmology & visual science · 2019Article
- Immune regulation in the aging retina.Progress in retinal and eye research · 2019Review
- Induction of Contrasuppressor Cells and Loss of Immune Privilege Produced by Corneal Nerve Ablation.Investigative ophthalmology & visual science · 2018Article
- The mucosal surfaces of both eyes are immunologically linked by a neurogenic inflammatory reflex involving TRPV1 and substance P.Mucosal immunology · 2018Article
- Role of Substance P Neuropeptide in Inflammation, Wound Healing, and Tissue Homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2017Review
- New insights into mononuclear phagocyte biology from the visual system.Nature reviews. Immunology · 2017Review
- Effect of Corneal Nerve Ablation on Immune Tolerance Induced by Corneal Allografts, Oral Immunization, or Anterior Chamber Injection of Antigens.Investigative ophthalmology & visual science · 2017Article
- Cellular and Molecular Mechanisms of Anterior Chamber-Associated Immune Deviation (ACAID): What We Have Learned from Knockout Mice.Frontiers in immunology · 2017Review
- Neuropeptide substance P and the immune response.Cellular and molecular life sciences : CMLS · 2016Review
- Unilateral muscle overuse causes bilateral changes in muscle fiber composition and vascular supply.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation in the eye is tightly regulated by multiple mechanisms that together contribute to ocular immune privilege. Many studies have shown that it is very difficult to abrogate the immune privileged mechanism called anterior chamber-associated immune deviation (ACAID). Previously, we showed that retinal laser burn (RLB) to one eye abrogated immune privilege (ACAID) bilaterally for an extended period of time. In an effort to explain the inflammation in the nonburned eye, we postulated that neuronal signals initiated inflammation in the contralateral eye. In this study, we test the role of substance P, a neuroinflamatory peptide, in RLB-induced loss of ACAID. Histological examination of the retina with and without RLB revealed an increase of the substance P-inducible neurokinin 1 receptor (NK1-R) in the retina of first, the burned eye, and then the contralateral eye. Specific antagonists for NK1-R, given locally with Ag within 24 h, but not 3, 5, or 7 d post-RLB treatment, prevented the bilateral loss of ACAID. Substance P knockout (KO) mice retained their ability to develop ACAID post-RLB. These data support the postulate that substance P transmits early inflammatory signals from the RLB eye to the contralateral eye to induce changes to ocular immune privilege and has a central role in the bilateral loss of ACAID. The possibility is raised that blocking of the substance P pathway with NK1-R antagonists postocular trauma may prevent unwanted and perhaps extended consequences of trauma-induced inflammation in the eye.
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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.