Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths. Roberts, L. B, Schnoeller, C., Berkachy, R., Darby, M., Pillaye, J., Oudhoff, M. J, Parmar, N., Mackowiak, C., Sedda, D., Quesniaux, V., Ryffel, B., Vaux, R., Gounaris, K., Berrard, S., Withers, D. R., Horsnell, W. G C, & Selkirk, M. E Science Immunology, 6(57):eabd0359, Science Immunology, mar, 2021. ![Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Innate lymphoid cells (ILCs) are critical mediators of immunological and physiological responses at mucosal barrier sites. Whereas neurotransmitters can stimulate ILCs, the synthesis of small-molecule neurotransmitters by these cells has only recently been appreciated. Group 2 ILCs (ILC2s) are shown here to synthesize and release acetylcholine (ACh) during parasitic nematode infection. The cholinergic phenotype of pulmonary ILC2s was associated with their activation state, could be induced by in vivo exposure to extracts of Alternaria alternata or the alarmin cytokines interleukin-33 (IL-33) and IL-25, and was augmented by IL-2 in vitro. Genetic disruption of ACh synthesis by murine ILC2s resulted in increased parasite burdens, lower numbers of ILC2s, and reduced lung and gut barrier responses to Nippostrongylus brasiliensis infection. These data demonstrate a functional role for ILC2-derived ACh in the expansion of ILC2s for maximal induction of type 2 immunity.
@article{Roberts2021,
abstract = {Innate lymphoid cells (ILCs) are critical mediators of immunological and physiological responses at mucosal barrier sites. Whereas neurotransmitters can stimulate ILCs, the synthesis of small-molecule neurotransmitters by these cells has only recently been appreciated. Group 2 ILCs (ILC2s) are shown here to synthesize and release acetylcholine (ACh) during parasitic nematode infection. The cholinergic phenotype of pulmonary ILC2s was associated with their activation state, could be induced by in vivo exposure to extracts of Alternaria alternata or the alarmin cytokines interleukin-33 (IL-33) and IL-25, and was augmented by IL-2 in vitro. Genetic disruption of ACh synthesis by murine ILC2s resulted in increased parasite burdens, lower numbers of ILC2s, and reduced lung and gut barrier responses to Nippostrongylus brasiliensis infection. These data demonstrate a functional role for ILC2-derived ACh in the expansion of ILC2s for maximal induction of type 2 immunity.},
author = {Roberts, Luke B and Schnoeller, Corinna and Berkachy, Rita and Darby, Matthew and Pillaye, Jamie and Oudhoff, Menno J and Parmar, Naveen and Mackowiak, Claire and Sedda, Delphine and Quesniaux, Valerie and Ryffel, Bernhard and Vaux, Rachel and Gounaris, Kleoniki and Berrard, Sylvie and Withers, David R. and Horsnell, William G C and Selkirk, Murray E},
doi = {10.1126/sciimmunol.abd0359},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Roberts et al. - 2021 - Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths.pdf:pdf},
issn = {2470-9468},
journal = {Science Immunology},
keywords = {OA,fund{\_}ack,original},
mendeley-tags = {OA,fund{\_}ack,original},
month = {mar},
number = {57},
pages = {eabd0359},
pmid = {33674321},
publisher = {Science Immunology},
title = {{Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths}},
url = {https://immunology.sciencemag.org/lookup/doi/10.1126/sciimmunol.abd0359},
volume = {6},
year = {2021}
}
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The cholinergic phenotype of pulmonary ILC2s was associated with their activation state, could be induced by in vivo exposure to extracts of Alternaria alternata or the alarmin cytokines interleukin-33 (IL-33) and IL-25, and was augmented by IL-2 in vitro. Genetic disruption of ACh synthesis by murine ILC2s resulted in increased parasite burdens, lower numbers of ILC2s, and reduced lung and gut barrier responses to Nippostrongylus brasiliensis infection. 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