AI Article Synopsis
- Innate lymphoid cells (ILCs), specifically group 2 ILCs (ILC2s), play a crucial role in immune response at mucosal surfaces, and recently, it has been discovered that they can produce the neurotransmitter acetylcholine (ACh).
- During parasitic nematode infections, ILC2s activate and release ACh, influenced by factors like interleukin-33 (IL-33) and IL-25, with additional enhancement from IL-2 when studied in the lab.
- Disabling ACh production in ILC2s leads to worse outcomes during infections, including more parasites, fewer ILC2s, and weakened defenses in the lungs and gut, highlighting the importance
Article 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 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 infection. These data demonstrate a functional role for ILC2-derived ACh in the expansion of ILC2s for maximal induction of type 2 immunity.
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| http://dx.doi.org/10.1126/sciimmunol.abd0359 | DOI Listing |
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