ArticlePLoS pathogens2015
The M3 muscarinic receptor is required for optimal adaptive immunity to helminth and bacterial infection.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- Selective modulation of murine intestinal MAmerican journal of physiology. Cell physiology · 2026Article
- Modulation of Master Transcription Factor Expression of Nile Tilapia Leukocytes via Cholinergic Pathways.International journal of molecular sciences · 2025Article
- Anti-muscarinic 3 antibodies associate with a severe clinical phenotype in patients with systemic sclerosis.Rheumatology (Oxford, England) · 2025Article
- Neuroimmune interactions: The bridge between inflammatory bowel disease and the gut microbiota.Clinical and translational medicine · 2025Review
- Helminth infection driven gastrointestinal hypermotility is independent of eosinophils and mediated by alterations in smooth muscle instead of enteric neurons.PLoS pathogens · 2024Article
- The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024Review
- Tuft cell acetylcholine is released into the gut lumen to promote anti-helminth immunity.Immunity · 2024Article
- Tuft cell-derived acetylcholine promotes epithelial chloride secretion and intestinal helminth clearance.Immunity · 2024Article
- T cells at the interface of neuroimmune communication.The Journal of allergy and clinical immunology · 2024Review
- The role of cellular and molecular neuroimmune crosstalk in gut immunity.Cellular & molecular immunology · 2023Review
- Neural innervation in adipose tissue, gut, pancreas, and liver.Life metabolism · 2023Review
- Tuft cell-derived acetylcholine regulates epithelial fluid secretion.bioRxiv : the preprint server for biology · 2023Article
- The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation.The Journal of investigative dermatology · 2022Article
- Microbial regulation of intestinal motility provides resistance against helminth infection.Mucosal immunology · 2022Article
- Differential Regulation of Allergic Airway Inflammation by Acetylcholine.Frontiers in immunology · 2022Article
- Immune Regulatory Roles of Cells Expressing Taste Signaling Elements in Nongustatory Tissues.Handbook of experimental pharmacology · 2022Article
- Paneth Cell Secretion in vivo Requires Expression of Tmem16a and Tmem16f.Gastro hep advances · 2022Article
- The intestinal neuro-immune axis: crosstalk between neurons, immune cells, and microbes.Mucosal immunology · 2021Review
- ILC3-derived acetylcholine promotes protease-driven allergic lung pathology.The Journal of allergy and clinical immunology · 2021Article
Corrections and comments
- Erratum issuedCorrection: The M3 muscarinic receptor is required for optimal adaptive immunity to helminth and bacterial infection.2015 · Culley, Fiona [corrected to Culley, Fiona Jane]
Authors and funding
13 authors.
Funding
Abstract
Innate immunity is regulated by cholinergic signalling through nicotinic acetylcholine receptors. We show here that signalling through the M3 muscarinic acetylcholine receptor (M3R) plays an important role in adaptive immunity to both Nippostrongylus brasiliensis and Salmonella enterica serovar Typhimurium, as M3R-/- mice were impaired in their ability to resolve infection with either pathogen. CD4 T cell activation and cytokine production were reduced in M3R-/- mice. Immunity to secondary infection with N. brasiliensis was severely impaired, with reduced cytokine responses in M3R-/- mice accompanied by lower numbers of mucus-producing goblet cells and alternatively activated macrophages in the lungs. Ex vivo lymphocyte stimulation of cells from intact BALB/c mice infected with N. brasiliensis and S. typhimurium with muscarinic agonists resulted in enhanced production of IL-13 and IFN-γ respectively, which was blocked by an M3R-selective antagonist. Our data therefore indicate that cholinergic signalling via the M3R is essential for optimal Th1 and Th2 adaptive immunity to infection.
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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.