ArticleThe Journal of experimental medicine2023
Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
The trial behind it
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.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Innate lymphoid cells in rheumatoid arthritis as mediators of pathology and resolution.Nature reviews. Rheumatology · 2026Review
- Review
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- SLC7A8 is essential for metabolic fitness and function of Th2 cells.The Journal of experimental medicine · 2026Article
- Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026Review
- ASNS-dependent asparagine availability supports intestinal ILC2 responses and type 2 immunity under nutrient-limited conditions.Frontiers in immunology · 2026Article
- Type 2 Inflammatory Diseases: The Crossroads of Immunity and Metabolism.Research (Washington, D.C.) · 2026Review
- Large neutral amino acid uptake and mTOR activation within CD4 T cells coordinate type 2 immunity and host resistance toDiscovery immunology · 2026Article
- L-Phenylalanine is a metabolic checkpoint of human Th2 cells.Cell reports. Medicine · 2025Article
- mTORC1 signaling in group 2 innate lymphoid cells coordinates neuro-immune crosstalk in allergic lung inflammation.Nature communications · 2025Article
- The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Metabolomic and functional analyses of small molecules secreted by intestinal nematodes in the activation of epithelial tuft cells.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025Review
- Tissue-Specific Metabolic Reprogramming in Innate Lymphoid Cells and Its Impact on Disease.Immune network · 2025Review
- High protein diet increases the risk of allergic sensitization but not asthma in mice through modulation of the cytokine milieu toward Th2 bias.The World Allergy Organization journal · 2025Article
- Immunometabolic analysis of primary murine group 2 innate lymphoid cells: a robust step-by-step approach.Frontiers in immunology · 2025Article
- Eating for immunity: how diet shapes our defenses.Current opinion in immunology · 2024Review
- Metabolic adaptations of ILC2 and Th2 cells in type 2 immunity.Current opinion in immunology · 2024Review
- Cooperation of ILC2s and TNature reviews. Immunology · 2024Review
- RNA helicase EIF4A1-mediated translation is essential for the GC response.Life science alliance · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the diet and invading pathogens-including helminths. Emerging evidence suggests ILC2 are acutely sensitive not only to canonical activating signals but also perturbations in nutrient availability. In the context of helminth infection, we identify amino acid availability as a nutritional cue in regulating ILC2 responses. ILC2 are found to be uniquely preprimed to import amino acids via the large neutral amino acid transporters Slc7a5 and Slc7a8. Cell-intrinsic deletion of these transporters individually impaired ILC2 expansion, while concurrent loss of both transporters markedly impaired the proliferative and cytokine-producing capacity of ILC2. Mechanistically, amino acid uptake determined the magnitude of ILC2 responses in part via tuning of mTOR. These findings implicate essential amino acids as a metabolic requisite for optimal ILC2 responses within mucosal barrier tissues.
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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.