ArticleCellular & molecular immunology2023
HTR2A agonists play a therapeutic role by restricting ILC2 activation in papain-induced lung inflammation.
Article in Cellular & molecular immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 19 citations in OpenAlex.
- Neural regulation in lung cancer: from mechanisms to new therapeutic perspectives.Clinical and experimental medicine · 2026Review
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Association between depressive symptom and respiratory health in two prospective cohort studies.NPJ primary care respiratory medicine · 2025Article
- Article
- Sexual dimorphism of lung immune-regulatory units imprint biased pulmonary fibrosis.Cellular & molecular immunology · 2025Article
- E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung.Scientific reports · 2025Article
- Tissue microenvironment induces tissue specificity of ILC2.Cell death discovery · 2024Review
- Serotonin suppresses lung ILC2 activation and proliferation.Cellular & molecular immunology · 2023Article
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Authors and funding
21 authors at 6 institutions in 2 countries.
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Abstract
Group 2 innate lymphoid cells (ILC2s) are a category of heterogeneous cells that produce the cytokines IL-5 and IL-13, which mediate the type 2 immune response. However, specific drug targets on lung ILC2s have rarely been reported. Previous studies have shown that type 2 cytokines, such as IL-5 and IL-13, are related to depression. Here, we demonstrated the negative correlation between the depression-associated monoamine neurotransmitter serotonin and secretion of the cytokines IL-5 and IL-13 by ILC2s in individuals with depression. Interestingly, serotonin ameliorates papain-induced lung inflammation by suppressing ILC2 activation. Our data showed that the serotonin receptor HTR2A was highly expressed on ILC2s from mouse lungs and human PBMCs. Furthermore, an HTR2A selective agonist (DOI) impaired ILC2 activation and alleviated the type 2 immune response in vivo and in vitro. Mice with ILC2-specific depletion of HTR2A (Il5
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