ArticleBlood2009
Proinflammatory tachykinins that signal through the neurokinin 1 receptor promote survival of dendritic cells and potent cellular immunity.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 74 citations in OpenAlex.
- Substance P receptor signaling contributes to host maladaptive responses during enteric bacterial infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Double-Edged Effects of Substance P in the Pathology of Alzheimer's Disease.Aging and disease · 2024Review
- Substance P receptor signaling contributes to host maladaptive responses during enteric bacterial infection.bioRxiv : the preprint server for biology · 2024Article
- From pain to tumor immunity: influence of peripheral sensory neurons in cancer.Frontiers in immunology · 2024Review
- Neurotransmitters: promising immune modulators in the tumor microenvironment.Frontiers in immunology · 2023Review
- Genetic Associations with Coronavirus Susceptibility and Disease Severity.Advances in experimental medicine and biology · 2023Review
- The diversity of neuroimmune circuits controlling lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Control of myeloid cell functions by nociceptors.Frontiers in immunology · 2023Review
- Enteroendocrine cells and gut hormones as potential targets in the crossroad of the gut-kidney axis communication.Frontiers in pharmacology · 2023Review
- Article
- 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
- Substance P-Friend or Foe.Journal of clinical medicine · 2022Article
- Review
- Lipoteichoic Acid fromNutrients · 2022Article
- Article
- A decision tree model for neuroimmune guidance of allergic immunity.Immunology and cell biology · 2021Review
- The Role of Neuropeptides in Pathogenesis of Dry Dye.Journal of clinical medicine · 2021Review
- Microarray patches enable the development of skin-targeted vaccines against COVID-19.Advanced drug delivery reviews · 2021Review
- Neurokinin receptors and their implications in various autoimmune diseases.Current research in immunology · 2021Review
- Substance P Release by Sensory Neurons Triggers Dendritic Cell Migration and Initiates the Type-2 Immune Response to Allergens.Immunity · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Dendritic cells (DCs) are the preferred targets for immunotherapy protocols focused on stimulation of cellular immune responses. However, regardless of initial promising results, ex vivo generated DCs do not always promote immune-stimulatory responses. The outcome of DC-dependent immunity is regulated by proinflammatory cytokines and neuropeptides. Proinflammatory neuropeptides of the tachykinin family, including substance P (SP) and hemokinin-1 (HK-1), bind the neurokinin 1 receptor (NK1R) and promote stimulatory immune responses. Nevertheless, the ability of pro-inflammatory tachykinins to affect the immune functions of DCs remains elusive. In the present work, we demonstrate that mouse bone marrow-derived DCs (BMDCs) generated in the presence of granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-4 (IL-4), express functional NK1R. Signaling via NK1R with SP, HK-1, or the synthetic agonist [Sar(9)Met(O(2))(11)]-SP rescues DCs from apoptosis induced by deprivation of GM-CSF and IL-4. Mechanistic analysis demonstrates that NK1R agonistic binding promotes DC survival via PI3K-Akt signaling cascade. In adoptive transfer experiments, NK1R-signaled BMDCs loaded with Ag exhibit increased longevity in draining lymph nodes, resulting in enhanced and prolonged effector cellular immunity. Our results contribute to the understanding of the interactions between the immune and nervous systems that control DC function and present a novel approach for ex vivo-generation of potent immune-stimulatory DCs.
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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.