Cited by 200Neuropeptides and Animal PhysiologyPain Mechanisms and TreatmentsNF-κB Signaling Pathways

Neurokinin‐1 receptor: functional significance in the immune system in reference to selected infections and inflammation

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Douglas, Steven D., Leeman, Susan E.·2011·Annals of the New York Academy of Sciences

Abstract

The G protein–coupled receptor (GPCR), neurokinin‐1 receptor (NK1R), and its preferred ligand, substance P (SP), are reviewed in relationship to the immune system and selected infections. NK1R and SP are ubiquitous throughout the animal kingdom. This important pathway has unique functions in numerous cells and tissues. The interaction of SP with its preferred receptor, NK1R, leads to the activation of nuclear factor‐kappa B (NF‐κB) and proinflammatory cytokines. NK1R has two isoforms, both a full‐length and a truncated form. These isoforms have different functional significances and differ in cell signaling capability. The proinflammatory signals modulated by SP are important in bacterial, viral, fungal, and parasitic diseases, as well as in immune system function. The SP–NK1R system is a major class 1, rhodopsin‐like GPCR ligand–receptor interaction.

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Crossref · 10.1111/j.1749-6632.2010.05826.x

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  • Substance P is involved in the initiation and transmission of itch through NK1R and MRGPRS expressed in the central nervous system and on various other cell types.

    “Substance P is involved in the initiation and transmission of itch through the neurokinin 1 receptor (NK1R)195,196 and the Mas-related G protein-coupled receptor (MRGPRS)197,198 expressed in the central nervous system and on various other cell types.”

    From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [196]

    The ‘Neurokinin 1 receptor’ section identifies NK1R as substance P’s preferred receptor and links their interaction to pain transmission. The ‘Substance P’ section reports substance P receptors on CNS cells. Neither passage establishes that the SP–NK1R pathway initiates or transmits itch; the separate MRGPRS citations are not attributed to this source. (LLM, conf=0.83)

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Authors
Douglas, S. D., & Leeman, S. E.
Affiliations
  • Children's Hospital of Philadelphia (US)
  • Boston University (US)
Corresponding author
Douglas, Steven D.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2010-11-22
Volume
1217
Issue
1
Pages
83-95
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W1599368877
Cited by
200
References
130
Citations by year
2026: 8 · 2025: 15 · 2024: 15 · 2023: 19 · 2022: 20 · 2021: 13 · 2020: 9 · 2019: 9 · 2018: 22 · 2017: 15 · 2016: 15 · 2015: 8 · 2014: 9 · 2013: 12 · 2012: 8
FWCI
0.64
Type
journal article
Language
en
Open access
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (P01MH076388, U01MH090325, R01MH049981)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
neurokinin-1 receptor, substance P, G protein-coupled receptors, immune system, inflammation, infection, NF-κB, inflammatory cytokines, receptor isoforms, bacterial infection, viral infection, fungal infection, parasitic infection
MeSH terms
Amino Acid Sequence, Animals, Humans, Infections, Inflammation, Molecular Sequence Data, Substance P, Receptors, Neurokinin-1, Inflammation Mediators, Protein Isoforms

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